Kategoriarkiv: Forskning og artikler

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Slump Test: Sensory Responses in Asymptomatic Subjects

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Om slump test for å finne ut av nevropatisk smerte eller betennelse.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2565641/

«While non-neural structures such as subcutaneous connective tissues, skin, blood vessels, and fascia may also be placed under increasing loads during neural tissue testing, Coppieters et al demonstrated that successive stages of the Slump Test did not alter the perception of experimentally induced muscle pain (i.e., non-neural pain). This finding provides some validation for use of the Slump Test in the examination of neural structures.»

«The procedure was divided into four stages:

  • SS—the subject was asked to put her hands behind her back, to slump at the mid- and lower back, and to tuck her chin into the chest, while the examiner placed his hand at the cervicothoracic junction to monitor cervical position (Figure 1.2);
  • KE—while maintaining the above position, the subject was asked to extend the left knee until full extension was reached (Figure 1.3);
  • AD—the subject was then asked to dorsiflex the left ankle (Figure 1.4);
  • CE—the subject was asked to maintain the lower limb position while the examiner removed his hand from the cervicothoracic junction and the subject extended the neck (Figure 1.5).
  • The subject was then asked to assume a comfortable sitting position and any residual responses were recorded (Figure 1.6). The examiner practised the test procedure several times on one subject to increase the consistency in test application prior to data collection.»

«All responses were located in the back or neck for the 29.8% of subjects who experienced a sensory response during SS, but for the subsequent three stages of the test, the vast majority of responses were located in the thigh, knee, or calf (Table 1)»

«A positive Slump Test implicates neural tissue as the source of symptoms. As found in this study, responses other than the presenting symptoms may simply be an artefact of the test, typical of the normal response in asymptomatic subjects; such responses must not be assumed to indicate a positive Slump Test. Bilateral comparison is advocated in interpreting this test.»

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Etiology of Myofascial Trigger Points

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Om triggerpunkter og hvordan muskelspenninger gir oksygenmangel som så fører til melkesyreopphopning. Nevner også at capillærer trekker seg sammen. En annen studie som det refereres til viser bilder og grafer av hvordan dette skjer; økt blodoppsamling pga trange kapillære vener der blodet strømmer ut fra triggerpunktet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3440564/#__ffn_sectitle

«Since the capillary blood pressure ranges from approximately 35 mm Hg at the beginning (arterial side) to 15 mm Hg at the end of the capillary beds (venous side), the capillary blood flow is temporarily obstructed during muscle contractions. The blood flow recovers immediately with relaxation, which is consistent with its normal physiological mechanism. In dynamic rhythmic contractions, intramuscular blood flow is enhanced by this contraction-relaxation rhythm, also known as the muscular pump. During sustained muscle contractions, however, muscle metabolism is highly dependent upon oxygen and glucose, which are in short supply.»

«Since oxygen and glucose are required for the synthesis of adenosine triphosphate (ATP), which provides the energy needed for muscle contractions, sustained contractions may cause a local energy crisis due to the lack of oxygen. To guarantee an adequate supply of ATP, the muscle can switch within a few seconds to anaerobic glycolysis. »

«Under anaerobic circumstances, however, most of the pyruvic acid produced during glycolysis is converted into lactic acid, thereby increasing the intramuscular acidity (pH). Most of the lactic acid diffuses out of the muscle into the bloodstream; post-exercise lactic acid is washed out within 30 minutes after exercise. Unfortunately, when the capillary circulation is restricted, as in sustained low-level contractions, this process comes to a standstill.»

«Small increases of the H+ concentration, as seen with inflammation, heavy muscle work, and ischemia, are sufficient to excite muscle group IV endings, contributing to mechanical hyperalgesia and central sensitization (15).»

«They identified 2 contributing factors, namely an increase in the volume of the vascular compartment, and an increased outflow resistance. Increased outflow resistance could be due to muscle contractures at the TrP that compress the capillary or venous bed. Sustained low-level contractions are common in the workplace where many occupations rely on prolonged postures, as seen in musicians, supermarket cashiers, computer operators, hairdressers, and dentists, among others.» Bilder ref til denne studies: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493167/

«Hägg suggested that the continuous activity of these motor units in sustained contractions causes overuse muscle fiber damage, especially to the Type I fibers during low-level activities, which he summarized in his Cinderella hypothesis21. It is conceivable that in sustained low-level contractions and in dynamic repetitive contractions, ischemia, hypoxia and insufficient ATP synthesis in type I motor unit fibers are responsible for increasing acidity, Ca2+ accumulation, and subsequently sarcomere contracture. Furthermore, starting with the sarcomere (super-) contraction, the intramuscular perfusion slows down and ischemia and hypoxia will occur. This may lead to the release of several sensitizing substances causing peripheral sensitization15,22.»

«A key factor is the local ischemia, which leads to a lowered pH and a subsequent release of several inflammatory mediators in muscle tissue. Hocking proposed an interesting counterargument, which deserves further exploration. Whether overuse mechanisms are the crucial initiating factor or persistent nociceptive input remains a point of debate and further study.»

Forklaring på hva Hocking mener:
«Rather than looking at overuse mechanisms, Hocking maintains that persistent nociceptive input causes the formation of TrPs through central sensitization of the C-fiber nociceptive withdrawal reflex and plateau depolarization of withdrawal agonist alpha-motor neurons and compensatory reticulospinal motor facilitation of antigravity muscles and plateau depolarization of withdrawal antagonist alpha-motor neurons (33). «

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The effects of neurodynamic mobilization on fluid dispersion within the tibial nerve at the ankle: an unembalmed cadaveric study

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Om hva nevropati og skader på nerver gjør, og hvordan neurodynamiske øvelser øker blodsirkulasjon internt i nerven. Nevner også hvordan skader, lav blodsirkulasjon og betennelser skaper sammensmeltninger i bindevevet mellom nerver og omliggende vev (muskler, skjelett, bindevev) som gjør at nervene ikke glir og dermed kan gi oss begrenset bevegelighet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3172954/

«These disorders include compression syndromes or other neuromuscular conditions that may be accompanied by neuropathic pain. Damaged nerves exhibit predictable pathophysiological responses including impaired nerve mobility, increased mechanosensitivity, impaired nerve conduction, nerve tissue ischemia, axonal transport inhibition, and intraneural edema.

The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version.  Impaired nerve mobility and increased mechanosensitivity provide the basis for existing studies of neurodynamic techniques. »

«Impaired nerve mobility and mechanosensitivity can be clinically assessed by measuring changes in joint range of motion, pain reproduction, or change of symptoms following neurodynamic mobilization.

«Intraneural edema is a common response to nerve injury, and is intimately involved in the proliferation of damage to nerve structure and function.

The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version. Edema is found in peripheral nerves that have been subject to trauma such as compression,excessive tension events, or vibration.  Even mild injury may result in epineurial edema,  but compression that is prolonged or of great magnitude leads to a breach of the diffusion barriers created by both the perineurium and microvasculature, resulting in endoneurial edema. The absence of lymphatic vessels in the endoneurium limits drainage of this edema, thereby creating a ‘mini-compartment syndrome’ within the nerve. »

«This ‘mini-compartment syndrome’, due to the increase in endoneurial pressure, subsequently leads to fibrosis and adhesions, impairing intrafascicular gliding. This loss of intrafascicular gliding creates an internal stretch lesion (Fig. 1). »

«The results showed significant mobilization effects in that there was increased fluid dispersion within the tibial nerve after the intervention. »

…de brukte bare kadavere i denne studien.
«The results showed significant mobilization effects in that there was increased fluid dispersion within the tibial nerve after the intervention. Because the tibial nerve was dissected free of all adjacent tissue and eliminated any external interfaces, the response to the mobilization appeared to be due to intraneural mechanics.»

Bevegelsene «pumper» internt i nerven og øker blodgjennomstreømning.
«During the mobilization technique, the tibial nerve alternately elongated and shortened which may have provided a temporary increase in intraneural pressure followed by a period of relaxation. Although speculative, it appears that this repetitive or ‘pumping’ action may have created a flushing of the dye and an alteration of the intraneural pressure as the intraneural fluid was dispersed.»

«In the early stages of stretch injury or compression, the ability to prevent or at least reduce edema may prevent or slow the inhibition of blood flow, thus preventing the sequelae leading to impaired axonal transport, demyelination, loss of elasticity due to fibrosis or adhesions, and ultimately to alteration in nerve structure and function. «

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Molecular profiling reveals synaptic release machinery in Merkel cells

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Ett par studier om Merkel celler som reagerer på vibrasjon med lav frekvens (5-30 Hz) som sier mange ting om deres funksjon. Den sier bl.a. at de utløser glutamate, som er et nevropeptid relatert til smertetilstander. Men den utløser også andre nevrotransmittere som nedregulerer andre sanse-nevroner. Pluss at den innerverer eptielceller.
http://m.pnas.org/content/101/40/14503.full

«These data indicate that Merkel cells are poised to release glutamate and neuropeptides.»

«Because the question of whether Merkel cells are sensory cells is unresolved, other functions have been proposed. For example, Merkel cells may play a passive role in touch by efficiently transmitting force to mechanosensitive afferents (12). Alternatively, they may release neuromodulators to regulate the sensitivity of mechanoreceptive neurons (20). Merkel cells have also been proposed to influence the development or innervation of epithelia (ref. 21, but see ref. 22).»

«Together, these data demonstrate that Merkel cells are excitable cells and designate glutamate and CCK8 as candidate neurotransmitters at synapses between Merkel cells and sensory afferents in vivo. Our conclusion that Merkel cells function as excitable cells is strengthened by the abundance of neuronal transcription factors that we found to be enriched in Merkel cells (Table 1).»

«How might neurotransmitter release be stimulated from Merkel cells? Merkel cells may be mechanoreceptive cells that are directly activated by touch. Alternatively, Merkel cells may receive input from active afferent terminals. The latter conjecture is bolstered by reports of reciprocal connections in Merkel cell-neurite complexes (11).»

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Are Chiropractic Tests for the Lumbo-Pelvic Spine Reliable and Valid? A Systematic Critical Literature Review

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Nevner forholdet mellom eksperter og ikke-eksperters vurdering av menneskekroppen.

http://www.sherman.edu/research/archives/Jclub/Hestbeck_Lebouf_critical%20review.pdf

«This reviews shows that when comparing students with clinicians (eg, Harvey [1991] and Jensen [1993]), the students consistently did best. When comparing “experts” (ie, Rhudy [1990]) with ordinary clinicians, the experts did not produce better results than ordinary clinicians and in some cases produced worse results. This may occur because the clinician develops idiosyncratic standards for the procedure.»

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Hypoxia-generated superoxide induces the development of the adhesion phenotype

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Viktig studie om mekanismen bak hvordan hypoxi gir arrvev (adhesions) i kroppen. Relatert til hyperventilering vil lite CO2 gir hypoxi og sammen med trange blodkar vil de utsatte stedene i kroppen utvikle arrvev mellom muskler og nerver. Nevner hvordan antioksidanter er viktig for å unngå arrvev, spesielt etter operasjoner. Og motsatt, at oksidanter kan skape arrvev fra friskt vev. Nevner også hvordan nitratreaksjoner er med å skaper arrvev, så mulig at CO2 bidrar med å dempe nitratreaksjonene og dermed dempe dannelsen av arrvev. Den viser også at det kan være mulig å få arrvev celler om til å bli normale celler.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574925/

«Adhesion fibroblasts exhibit higher TGF-β1 and type I collagen expression as compared to normal peritoneal broblasts. Furthermore, exposure of normal peritoneal fibroblasts to hypoxia results in an irreversible increase in TGF-β1 and type I collagen. We postulated that the mechanism by which hypoxia induced the adhesion phenotype is through the production of superoxide either directly or through the formation of peroxynitrite. »

«Hypoxia treatment resulted in a time-dependent increase in TGF-β1 and type I collagen mRNA levels in both normal peritoneal and adhesion fibroblasts.»

«In contrast, treatment with SOD, to scavenge endogenous superoxide, resulted in a decrease in TGF-β1 and type I collagen expression in adhesion fibroblasts to levels seen in normal peritoneal fibroblasts; no effect on the expression of these molecules was seen in normal peritoneal fibroblasts. »

«In conclusion, hypoxia, through the production of superoxide, causes normal peritoneal fibroblasts to acquire the adhesion phenotype. Scavenging superoxide, even in the presence of hypoxia, prevented the development of the adhesion phenotype. These findings further support the central role of free radicals in the development of adhesions.»

«Postoperative adhesions are a significant source of impaired organ functioning, decreased fertility, bowel obstruction, difficult reoperation, and possibly pain (1,2)

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Destroy user interface c»

«The processes that result in either normal peritoneal tissue repair or the development of adhesions include the migration, proliferation, and/or differentiation of several cell types, among them inflammatory, immune, mesothelial, and fibroblast cells (3)

«Hypoxia, resulting from tissue injury, has been suggested to play an important role in wound healing, and may therefore be a critical factor in the development of postoperative adhesions (4,7)

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Destroy user interface contrHypoxia is known to trigger the expression of TGF-β1, which consequently increases the expression of extracellular matrix proteins, including type I collagen (4) 

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Destroy user interface contr«Type I collagen synthesis has been shown to be crucially dependent on the availability of molecular oxygen in tissue culture, animal, and human wound healing experiments (8,9)

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Destroy user interface controlMoreover, exposure of normal peritoneal fibroblasts to hypoxia irreversibly induces TGF-β1 and type I collagen to levels seen in adhesion fibroblasts (4,10)

«Additionally, hypoxia is known to acutely promote superoxide (O2.−) generation from disparate intracellular sources that include xanthine dehydrogenase oxidase (11), mitochondrial electron transport chain (12), and NAD[P]H oxidase (13).

In biological systems, superoxide dismutase (SOD) protects against the deleterious actions of this radical by catalyzing its dismutation to hydrogen peroxide plus oxygen, (14) Whereas SOD breaks down O2.−, xanthine oxidase synthesizes O2.−. Xanthine oxidase appears to be one of the major superoxide-producing enzymes (14)«

«Scavenging superoxide restores both TGF-β1 and type I collagen mRNA levels in adhesion fibroblasts to levels observed in normal peritoneal fibroblasts»
«Normal peritoneal and adhesion fibroblasts treated with super-oxide dismutase, a O2.− scavenging enzyme, exhibited a dose–response decrease (0, 5, 10, 15, and 20 units/ml) in TGF-β1 and type I collagen mRNA levels in adhesion fibroblasts while not effecting normal peritoneal fibroblasts (Figs. 3A and B).»

«Scavenging superoxide during hypoxia exposure protects against the development of the adhesion phenotype»

«Peroxynitrite treatment increased the adhesion phenotype markers, TGF-β1 and type I collagen»

«Adhesion fibroblasts are myofibroblasts, defined as transiently activated fibroblasts exhibiting features intermediate between those of smooth muscle cells and fibroblasts, including the expression of α-SM actin (29,21) and a depleted antioxidant system (22). In normal wound healing, as the wound resolves, the cellularity decreases and the myofibroblasts disappear by apoptosis (23). However, in several pathological cases, including fibrosis, myofibroblastic differentiation persists and causes excessive scarring (24,25).»

«This is further supported by the fact that when O2.− was scavenged, there was in a significant decrease in TGF-β1 and type I collagen in adhesion fibroblasts to levels seen in normal peritoneal fibroblasts. »

«Reactive oxygen species (ROS) are involved in TGF-β-stimulated collagen production in murine embryo fibroblasts (NIH3T3), and the effect of glutathione depletion on TGF-β-stimulated collagen production may be mediated by facilitating ROS signaling (37).»

«Reactive oxygen and nitrogen intermediates control the synthesis of cytokines and growth factors in several in vitro models (40). For instance, they modulate the expression and/or release of monocyte chemoattractant protein-1 (41,42), tumor necrosis factor-α, interleukin (IL)-1 (43,44), IL-8 (45,46), platelet-derived growth factor (47,48), and TGF-β1 (49). «

«Adhesion fibroblasts exhibited a significantly lower level of nitric oxide (NO) and higher protein nitration as compared to normal peritoneal fibroblasts, although there was no difference in the iNOS expression level between the two cell lines (17,50,51). This strongly indicates that adhesion fibroblasts use NO to form ONOO−, and consequently their basal ONOO− levels are higher than normal peritoneal fibroblasts. «

«Thus, treatment with SOD might affect the homeostasis of myofibroblasts by inducing cell death or the phenotypic reversion of myofibroblasts into normal fibroblasts. »

«Our results clearly indicate that hypoxia generated O2.− is a key player in the formation of the adhesion phenotype. This became evident when normal peritoneal fibroblasts were treated with SOD under hypoxic conditions and no change in adhesion markers was seen.»


«In this model, hypoxia-generated O2.− exerts its effect directly by enhancing the expression of TGF-β1, which consequently leads to elevated levels of type I collagen, a hallmark of the adhesion phenotype.»

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Neuromuscular strain as a contributor to cognitive and other symptoms in chronic fatigue syndrome: hypothesis and conceptual model

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Viktig studie om nervesystemet og bindevevets «adhesions» som bidragsyter til smerte.

http://www.frontiersin.org/Integrative_Physiology/10.3389/fphys.2013.00115/full

«Work by Brieg, Sunderland, and others has emphasized the ability of the nervous system to undergo accommodative changes in length in response to the range of limb and trunk movements carried out during daily activity. If that ability to elongate is impaired—due to movement restrictions in tissues adjacent to nerves, or due to swelling or adhesions within the nerve itself—the result is an increase in mechanical tension within the nerve. »

«This adverse neural tension, also termed neurodynamic dysfunction, is thought to contribute to pain and other symptoms through a variety of mechanisms. These include mechanical sensitization and altered nociceptive signaling, altered proprioception, adverse patterns of muscle recruitment and force of muscle contraction, reduced intra-neural blood flow, and release of inflammatory neuropeptides. »

«In our clinical work, we have found that neuromuscular restrictions are common in CFS, and that many symptoms of CFS can be reproduced by selectively adding neuromuscular strain during the examination.»

«As defined by Yunus, central sensitivity is “clinically and physiologically characterized by hyperalgesia (excessive sensitivity to a normally painful stimulus, e.g., pressure), allodynia (painful sensation to a normally non-painful stimulus, e.g., touch and massage), expansion of the receptive field (pain beyond the area of peripheral nerve supply), prolonged electrophysiological discharge, and an after-stimulus unpleasant quality of pain (e.g., burning, throbbing, numbness)” (Yunus, 2008).»

«These symptoms might be mediated by amplified central sensitivity, but peripheral factors, which have been described in FM and irritable bowel syndrome (IBS), may also play a role (e.g., Price et al., 2009; Staud et al., 2009). »

«Staud has shown that local anesthetic injection into trapezius muscle tender points results in lower levels of thermal hyperalgesia in the forearm, consistent with peripheral nociceptive input as a contributor to central sensitization (Staud et al., 2009).»

«The interaction of nerve mechanics and function has been termed neurodynamics. As an example of the principles of neurodynamics, the median nerve elongates approximately 20% as the upper extremity moves from a position of full wrist and elbow flexion to one of full wrist and elbow extension (Butler, 1991). »

» If that ability to elongate is impaired—due to movement restrictions in tissues adjacent to the median nerve and its branches, or due to swelling or adhesions within the median nerve itself—the result is an increase in mechanical tension within the nerve. This adverse neural tension, also termed neurodynamic dysfunction, is thought to contribute to pain and other symptoms through mechanical sensitization and altered nociceptive signaling, altered proprioception, adverse patterns of muscle recruitment and force of muscle contraction, reduced intra-neural blood flow, and release of inflammatory neuropeptides (Lindquist et al., 1973; Kornberg and McCarthy, 1992;Shacklock, 1995; Slater and Wright, 1995; Balster and Jull, 1997; Van der Heide et al., 2001; Kobayashi et al., 2003; Orlin et al., 2005).»

«It is now well-established that manual stretch of nerves is capable of evoking increased sweating and alterations of blood flow in peripheral tissues, providing evidence of electrophysiologic activity in sympathetic nerve fibers (Lindquist et al., 1973; Kornberg and McCarthy, 1992; Slater and Wright, 1995; Orlin et al., 2005). Conversely, treatment of areas of adverse neural tension (for example in carpal tunnel syndrome, cervico-brachial pain, and osteoarthritis) leads to improved functional outcomes (Rozmaryn et al., 1998; Deyle et al., 2000; Tal-Akabi and Rushton, 2000;Akalin et al., 2002; Allison et al., 2002).»

«The most notable examples of these provocation maneuvers are ankle dorsiflexion, the passive straight leg raise test, the upper limb tension (or neurodynamic) tests, and the seated slump test (Butler, 1991,2000). Test-retest reliability is good for straight leg raise, slump testing, and upper limb neurodynamic testing. (Coppieters et al., 2001;Herrington et al., 2008)»

«Because it is not possible to differentiate completely between adverse neural tension and strain in muscles, fascia, and other soft tissues, we will use the more general term “neuromuscular strain” in this paper. »

«As shown on the left in Figure 1, neuromuscular strains and movement restrictions can develop as a result injuries and activities of daily life (for example, due to soft tissue and peri-neural adhesions around scars, contusions and fractures that reduce range of motion, anatomic abnormalities like scoliosis and kyphosis, overuse injuries, and others).»

«If the neuromuscular strains were not treated, and if the individual adapted to the increased symptom burden with decreased activity, then neural, soft tissue and muscular restrictions would be expected to worsen, leading to greater impairment and greater central sensitization. »

«In our clinical work, we have found that neuromuscular restrictions are common in CFS.»
«We have also noted that many symptoms of CFS can be reproduced by selectively adding neuromuscular strain during the examination (Rowe et al., 2013a,b). »

«Despite the elevation of the leg, which might have been expected to improve venous return to the heart and thereby improve blood flow to the brain, lightheadedness increased, as did visual blurring. Both individuals remained more fatigued than usual for 12–24 h. Thus, supine neuromuscular strain provoked increased fatigue and cognitive disturbance, the two symptoms not adequately explained by the central sensitivity hypothesis thus far.»

«We have observed that open treatment of these movement restrictions using manual therapy is associated with clinical improvement (Rowe et al., 2013a,b).»

«The hypothesis can be tested by evaluating the whether the response to a given neuromuscular strain differs between CFS subjects and controls with regard to immediate and delayed (24-h) symptoms, and with regard to measures of central sensitivity, such as changes in heart rate variability, or changes in pain sensitivity as measured by pressure-pain thresholds. «

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Recognition of central sensitization in patients with musculoskeletal pain: Application of pain neurophysiology in manual therapy practice

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Nevner det aller meste om sentral sensitering og hvordan de gjenkjennes i klinisk praksis.

http://www.thblack.com/links/RSD/ManTher2010_15_135_CSinMusculoskelPain-PainNeurophys.pdf

«Even with acute pain the nervous system undergoes some changes. When tissue is damaged and pain persists for a few days with adaptation of unimodal nociceptors, the responsiveness of polymodal nociceptive endings is enhanced by substances released from various sources (i.e. serotonin released by platelets) (Purves et al., 1997). This process is called primary hyperalgesia or peripheral sensitization of nociceptors, and represents a protective action by the human body in order to prevent further use of damaged structures and consequent further damage of the traumatized and surrounding tissues.»

«Secondary hyperalgesia refers to increased responsiveness of dorsal horn neurons localized in the spinal segments of the primary source of nociception.»

«Central sensitization is defined as an augmentation of responsiveness of central neurons to input from unimodal and polymodal receptors (Meyer et al., 1995). Central sensitization encompasses altered sensory processing in the brain (Staud et al., 2007), malfunctioning of descending anti-nociceptive mechanisms (Meeus et al., 2008), increased activity of pain facilitatory path- ways, temporal summation of second pain or wind-up (Meeus and Nijs, 2007; Staud et al., 2007), and long-term potentiation of neuronal synapses in the anterior cingulate cortex (Zhuo, 2007).»

«The presence of central sensitization in patients with musculoskeletal pain implies an increased complexity of the clinical picture (i.e. an increase in unrelated symptoms and hence a more difficult clinical reasoning process) (Nijs et al., 2009), as well as decreased odds for a favorable rehabilitation outcome (Jull et al., 2007).»

«Central sensitivity syndromes is a term first used by Yunus in 2000 to describe a group of overlapping conditions bound by a common pathophysiological mechanism of central sensitization (Yunus, 2007a).»

«Another example is chronic non-specific low back pain. Some studies provided evidence in support of the presence of central sensitization in patients with non-specific chronic low back pain (Giesecke et al., 2004; Schmidt-Wilcke et al., 2006), while others refute such an association (Hoffman et al., 2005; Julien et al., 2005). It is concluded that central sensitization is present in some cases of chronic non-specific low back pain, possibly representing one of the subgroups of this frequent musculoskeletal disorder (Wand and O’Connell, 2008).»

«The myofascial variety within the heterogeneous group of temporomandibular disorders is also characterized by central sensitization (Yunus, 2007a). Likewise, regional chronic pain conditions that present with tender and/or trigger points in the absence of structural pathology (frequently referred to as myofascial pain syndrome) should alert the manual therapist to the possibility that central sensitization is determining the clinical picture (Yunus, 2007a). However, to our knowledge available evidence in support of central sensitization in patients with myofascial pain syndrome is limited to chronic whiplash associated disorders, temporoman- dibular disorders and chronic non-specific low back pain.»

«Furthermore, various subgroups of headache, chronic tension-type headache (Langemark et al., 1993; Pielsticker et al., 2005) and migraine (Burnstein et al., 2000; Weissman-Fogel et al., 2003) can be viewed as central sensitivity syndromes. Finally, rheumatoid arthritis and osteoarthritis are examples of local musculoskeletal disorders possibly causing continuous activation of polymodal nociceptors that initiate or sustain central sensitization (Yunus, 2007a).»

table1

«Central sensitization entails much more than generalized hypersensitivity to pain: it is characterized by an increased responsiveness to a variety of stimuli including mechanical pressure (Desmeules et al., 2004), chemical substances (Morris et al., 1997), cold temperature (Kasch et al., 2005), heat temperature (Meeus et al., 2008), electrical stimuli (Banic et al., 2004; Desmeules et al., 2004), stress, emotions, and mental load. The clinical picture is suggestive of a general intolerance to all kinds of physical and emotional stressors and hence a large decreased load tolerance of the human body in general.»

table2

«An ongoing source of peripheral nociception is required before the process of peripheral sensitization can establish central sensitization (Nijs and Van Houdenhove, 2009). Tissue injury healing and focal pain recovery should occur as soon as possible to prevent development of central sensitization (Vierck, 2006).»

«One of the main characteristics of central sensitization in patients with musculoskeletal pain is a generalized rather than a localized decrease in their pressure pain threshold. Here, ‘generalized’ implies more than a segmental spreading of the symptom area, in that it means that the increased sensitivity is localized at sites segmentally unrelated to the primary source of nociception (e.g. the lower limbs in case of a whiplash trauma).»

«Lower pressure pain thresholds at symptomatic areas most often represent primary hyperalgesia due to sensitized polymodal noci- ceptors within injured musculoskeletal structures. By measuring pressure pain thresholds outside the area of primary nociception, widespread hyperalgesia or secondary hyperalgesia can be detec- ted.»

«In cases of secondary hyperalgesia, a reduced pressure pain threshold in the various tissues innervated by the same segment (or two neighboring segments) can be detected.»

«Findings of numerous areas of hyperalgesia at sites outside and remote from the symp- tomatic site, together with a non-segmental general decrease in pressure pain threshold, may imply a generalized hyperexcitability of central nociceptive pathways (Sterling et al., 2004).»

«Pressure algometry provides a reliable and valid measure of the pressure pain threshold (Vanderweeen et al., 1996; Farasyn and Meeusen, 2003). In the absence of a pressure algometer, manual palpation can be used. Even when a manual therapist is not sus- pecting central sensitization, the finding of generalized hypersen- sitivity to manual palpation during routine clinical examination should alert the clinician.»

«Like every other tissue in the human body, peripheral nerves and nervous tissues (including connective tissue) themselves can become hypersensitive to mechanical stimuli such as tension and pressure.»

«Besides the passive tests listed above (Table 3), altered sensory processing can be demonstrated during exercise. Pain thresholds increase during physical activity in healthy individuals and can stay augmented for up to 30 min post-exercise. This is the result of endogenous opioid release (Koltyn and Arbogast, 1998) and related activation of several (supra)spinal anti-nociceptive mechanisms such as the adrenergic and serotonergic pathways (Millan, 2002).»

 

«Stress (particularly when chronic) may well trigger lower pain thresholds. This was demonstrated by Suarez-Roca et al. (2008) who reported reduced GABA neurotransmission and consequent hyperalgesia in rats after repeated forced swimming stress.»

«A constant or decreased pain threshold during and following exercise suggests malfunc- tioning of these anti-nociceptive mechanisms (Whiteside et al., 2004) and hence central sensitization. An abnormal pain threshold response to exercise should be regarded as one of the many possible signs of central sensitization.»

table4

 

 

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PROLONGED ALTERATION OF VASOCONSTRICTOR AND VASODILATOR RESPONSES IN RAT KNEE JOINTS BY ADJUVANT MONOARTHRITIS

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Viktig bekreftelse på at blodsirkulasjon hemmes i betente ledd og at dette er noe av utgangspunktet for slitasjeskader siden vevet og skjelettet ikke får de næringsstoffene de trenger. Viktig studie å se på men vanskelig å copy-paste sitater…

Klikk for å få tilgang til 349.full.pdf

«These vasoactive responses were completely abolished in the chronically inflamed knee joint, the abolition persisting throughout the investigation. »

«Since articular cartilage is critically dependent on synovial fluid formation for its nutrition, loss of neurovascular control of the synovial microcirculation could contribute to the degenerative changes that commonly accompany chronic inflammatory joint diseases.»

«The role of synovial nerves in the development of various forms of acute inflammation has previously been reported (Lam & Ferel,1991)and it is thought that their efects may be mediated by local release of SP, which is known to be pro-inflammatory in this region.»

«These experiments showed that electrical stimulation of nerves supplying the rat knee joint caused a frequency-dependent constriction of articular bloodvesels, and that topical aplication of SP to the exposed joint surface produced a potent vasodilatation, although this particular effect was found to be transient.»

Viser at nervesignaler gjør at blodkar trekker seg sammen i leddet. Kan henvise til at et overstimulert nervesystem (sympaticus dominans) trekker blodkar sammen.

«A highly significant frequency-dependent decrease in joint bloodflow occurred in normal rats when electrical stimulation of the saphenous nerve was performed (P < 0 001, repeated measures one-way ANOVA; n = 10). The greatest vasoconstriction resulted when 30 Hz stimulation was applied to the nerve: this elicited a 37.3+7.3% fall in perfusion.»

Nevner at Substans P gir vasodilasjon (37%) umiddelbart, men at det over tid gir en vasokonstriksjon (40%).
«Substance P, when applied topically to the exposed surface of normal knee joints, produced a significant dose-dependent augmentation of joint bloodflow (P<0.001;n= 10), culminating in a peak rise of 45*1+8*6% with the10-9 mol dose.»
«At week 1, SP had no significant effect on synovial blood flow (P= 0.511;n= 10),but at week 3 vasoconstriction was recorded (P< 0*001;n= 9); at both these times the results were significantly different from those of normal rats (P < 0.001). A fall of articular perfusion of about 40% occurred at week 3 when 10-8 and10-t2 mol of SP was administered to the joint, but the intermediate doses produced less efect. »

Nevner at blodsirkulasjonen er dårlig i over 3 uker etterpå, selv om betennelsen er borte.
«Since articular cartilage is dependent on the synovial perfusion (McKibbin& Maroudas, 1979), this initial reduction in joint blood flow could cause the integrity of the joint to deteriorate and lead to degenerative changes. It has previously been shown that adjuvant- induced inflammation in the rat knee joint abolishes sympathetic vasoconstriction and the neuropeptidergic vasodilator response to SP at 1week post-treatment (McDougall et al. 1994).The investigation outlined here has shown that these alterations are not transitory, and are stil present 3 weeks after injection of adjuvant, even though the inflammatory process appears to be abating by then.»

Nevner at det blir vasokonstriksjon når det er betennelse samtidig.
«Chronically inflamed joints did not show vasodilatation in response to SP at any stage; indeed there was some evidence of vaso- constriction. This finding suggests that the SP receptors are either radically transformed or possibly inactivated by the inflammatory process.»

«Comparing this finding with that of the present study, it would appear that the integrity of sympathetic transmission and SP receptor activation in rat knee joints declines as inflammation becomes more chronic. Loss of these neurovascular controls could contribute to the degenerative changes that commonly accompany chronic inflammatory joint diseases.»