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Skin Matters: Identifying Pain Mechanisms and Predicting Treatment Outcomes

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Mye om huden relatert til smerte og nevropati! Mest relatert til biopsi, men mye kan knyttes til behandling også. Spesielt ved hemming av TRPV1.

http://www.hindawi.com/journals/nri/2013/329364/

This data has led to new insights into the potential pain mechanisms for various pain conditions including neuropathic pain (from small fiber neuropathies) and Complex Regional Pain Syndrome. The somatosensory neurons that innervate our skin constantly update our brains on the objects and environmental factors that surround us. Cutaneous sensory neurons expressing nociceptive receptors such as transient receptor potential vanilloid 1 channels and voltage-gated sodium channels are critical for pain transmission. Epidermal cells (such as keratinocytes, Langerhans cells, and Merkel cells) express sensor proteins and neuropeptides; these regulate the neuroimmunocutaneous system and participate in nociception and neurogenic inflammation.

The skin has homeostatic and immunologic barrier functions, but acts as a complex sensory organ as well [1]. The somatosensory neurons that innervate our skin constantly update our brains on the objects and environmental factors that surround us [2]. The neuroimmunocutaneous system (NICS) is responsible for the cutaneous sensations of touch, pressure, temperature, and pain. This sensory transduction occurs via primary afferent nerves following reciprocated signals between neuronal and nonneuronal skin cells of the NICS [1]. New data concerning peripheral pain mechanisms from within the skin have led to new insight into the potential pain mechanisms for various pain conditions including neuropathic pain syndromes such as diabetic neuropathy and Complex Regional Pain Syndrome.

In pain and neurogenic inflammation, TRPV1 is coexpressed on TRPA1-expressing sensory nerves; both integrate a variety of noxious stimuli [4]. Complex signaling pathways between cells of the NICS, such as keratinocytes, TRPV1-expressing nociceptors, and macrophages, lead to the release of neural growth factor (NGF), prostaglandins, opioids, proinflammatory cytokines, and chemokines [1]. These lead to sensitisation of the peripheral nerves by upregulating ionic channels and by inducing further spinal cord cytokine release [8].

2. Small Fiber Neuropathy (SFN)
Neuropathic pain arises as a direct consequence of a lesion or disease of the somatosensory system; it affects about 7% of the general population [10, 11].

Small fiber neuropathy is a neuropathy of the small nonmyelinated fibers and myelinated A delta fibers. Neuropathic pain occurs from small fiber neuropathy; small fiber neuropathy is caused by a wide variety of acquired and genetic disorders [12], many of which are treatable [13].

Diabetes mellitus is the most frequent underlying cause of SFN [14]. Other causes include toxic (e.g., alcohol), metabolic, immune-mediated, infectious, and hereditary causes.

About 60% of patients describe the painful sensation as spontaneous (burning, sunburn-like, paroxysmal, pruritic, and deep), with worsening at rest or during the night [12]; the sensation can be associated with thermal evoked pain (cold or warm) with or without allodynia, a painful response to a normally innocuous stimulus, and hyperalgesia, an increased response to a painful stimulus [12]. In addition there are negative sensory symptoms (thermal and pinprick hypoesthesia) that reflect peripheral deafferentation [19]. Sensation of cold feet is reported, though warm to touch. Thermal hypoesthesia with or without pinprick hypoesthesia has been detected in 40% of patients [20]; hyperalgesia and aftersensation have been detected in 10–20% of patients [12, 20].

2.3. Complex Regional Pain Syndrome (CRPS)
CRPS is a syndrome characterized by a continuing (spontaneous and/or evoked) regional pain, that is, seemingly disproportionate in time or degree to the usual course of any known trauma or other lesion [23]. The pain is regional (not in a specific nerve territory or dermatome); it usually has a distal predominance of abnormal sensory, motor, sudomotor, vasomotor, and/or trophic findings. It has signs of central sensitisation such as allodynia and hyperalgesia. The syndrome shows variable progression over time [23].

Accumulating experimental and clinical evidence supports the hypothesis that Complex Regional Pain Syndrome type I (CRPS-I) might indeed be a small fiber neuropathy [25]. Most post-traumatic inflammatory changes observed in CRPS are mediated by two peptides, CGRP and substance P [26]. The activation of cutaneous nociceptors can induce retrograde depolarisation of small-diameter primary afferents, causing release of neuropeptides such as substance P and CGRP from sensory terminals in the skin.

A specific diagnostic test for small fiber neuropathy is a skin biopsy; this includes a count of the intraepidermal small nerve fibers (IENF) that cross the basal membrane. The loss of IENF can be reliably measured and is currently used to diagnose small fiber neuropathy (SFN) [17].


Skin biopsy is much less invasive and more practical than peripheral nerve biopsy. It is a safe and reliable tool for investigating nociceptive fibers in human epidermis and dermis [29]. It can be performed at any site of the body, with a disposable punch, using a sterile technique, and under local anesthesia (Figure 2) [29].

A recent study assessed the usefulness of skin biopsy in the assessment of 145 patients with suspected SFN [21]. In 59% of patients skin biopsy was abnormal in at least one site [21]. Patients with confirmed SFN were significantly more likely to have pain; they were more than twice as likely to respond to standard neuropathic pain medications [21]. A positive response to neuropathic pain medications was seen in 84% of patients with an abnormal skin biopsy compared to only 42% of those with a normal biopsy [21]. Skin biopsy has a relatively high yield in patients with sensory symptoms with no findings of mixed fiber neuropathy on clinical examination or on nerve conduction studies [21].

Along with neuronal and immunological systems, the skin plays a critical role in sensory transduction [1]. Further direct targeting of the skin with topical agents should be considered. The interaction of TRPV1 and TRPA1 channels in the skin in painful conditions needs further exploration. Second generation TRPV1 antagonists (without on-target side effects of hyperthermia and burn risk) are under development [6].

In Pain Medicine, the skin does indeed matter!

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Pathophysiology of Nerve Compression Syndromes: Response of Peripheral Nerves to Loading

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Om nerve compression syndrome, som sannsynligvis er årsaken til de fleste plager folk kommer til behandling for. Nevner hvordan nervevev påvirkes i løpet av timer, dager og uker. Nevner de 3 gradene av kompresjon og hvilke symptomer de gir.

http://ergo.berkeley.edu/docs/1999rempeljbjs.pdf

Nerve compression syndromes involve peripheral- nerve dysfunction that is due to localized interference of microvascular function and structural changes in the nerve or adjacent tissues.

When tissues are subjected to load or pressure, they deform and pressure gradients are formed, redistribut- ing the compressed tissue toward areas of lower pres- sure. Nerve compression syndromes usually occur at sites where the nerve passes through a tight tunnel formed by stiff tissue boundaries. The resultant con- fined space limits movement of tissue and can lead to sustained tissue pressure gradients. Space-occupying structures or lesions (for example, lumbrical muscles, tu- mors, and cysts) can cause nerve compression injury, as can conditions associated with accumulation of fluid (for example, pregnancy, congestive heart failure, and muscle compartment syndromes) or accumulation of extracellular matrix (for example, acromegaly, myx- edema hypothyroidism, and mucopolysaccharidosis)76.

Although nerve injuries related to vibration occur near the region of exposure, the symptoms may be manifest at another site, where the nerve may be constricted.

Other conditions, such as diabetes mellitus, may increase the likelihood that a compressed nerve will undergo a pathological response. In addition, there may be an in- flammatory reaction that may impair the normal gliding of the nerve.

Lying next to the myelinated nerve fibers are many nonmyelinated fibers associated with one Schwann cell. Myelinated and nonmyelinated nerve fibers are organized in bundles, called fascicles, which are surrounded by a strong membrane called the peri- neurial membrane, consisting of laminae of flattened cells.

Between the nerve fibers and their basal mem- brane is an intrafascicular connective tissue known as the endoneurium. The quantity of the connective-tissue components may vary between nerves and also along the length of the same nerve. For example, nerves lo- cated superficially in the limb or parts of the nerve that cross a joint contain a greater quantity of connective tissue, possibly as a response to repeated loading76.

The propagation of impulses in the nerve fibers as well as the communication and nutritional transport sys- tem in the neuron (axonal transport) requires an ade- quate energy supply. Therefore, the peripheral nerve contains a well developed microvascular system with vascular plexuses in all of its layers of connective tis- sue36,38. The vessels approach the nerve trunk segmen- tally and have a coiled configuration so that the vascular supply is not impaired during normal gliding or excur- sion of the nerve trunk. When the vessels reach the nerve trunk, they divide into branches that run longi- tudinally in various layers of the epineurium and they also form numerous collateral connections to vessels in the perineurial sheath. When the vessels pass through the perineurium into the endoneurium, which contains primarily capillaries, they often go through the perineu- rium obliquely, thereby constituting a possible valve mechanism36,38.

The perineurial layer and the endoneurial vessels play an important role in protecting the nerve fibers in the fascicles. The endoneurial milieu is protected by a blood-nerve barrier, and the tissue pressure in the fascicle (endoneurial fluid pressure) is slightly positive50.

The median and ulnar nerves may glide 7.3 and 9.8 millimeters, respectively, during full flexion and extension of the elbow, and the extent of excursion of these nerves just proximal to the wrist is even more pronounced (14.5 and 13.8 millimeters, respectively)90. In relation to the flexor retinaculum, the median nerve can move a maximum of 9.6 millimeters during wrist flexion and somewhat less during wrist extension; it also moves during motion of the fingers48.

Acute Effects of Nerve Compression (Effects within Hours)
In animal experiments, low-magnitude extraneural compression was noted to decrease intraneural micro- vascular flow, impair axonal transport, and alter nerve structure and function. Extraneural pressures of 2.7 kilo- pascals (twenty millimeters of mercury), induced with use of miniature inflatable cuffs, reduced epineurial ve- nule blood flow68. At pressures of 10.7 kilopascals (eighty millimeters of mercury), all intraneural blood flow ceased. Similarly, pressures of 4.0 kilopascals (thirty mil- limeters of mercury) inhibited both fast and slow ante- grade as well as retrograde axonal transport8.

In subjects with different blood pres- sures, the critical extraneural pressure threshold above which nerve function was blocked was 4.0 kilopascals (thirty millimeters of mercury) less than the diastolic pressure. This finding, combined with the observation that carpal tunnel syndrome may manifest with the treat- ment of hypertension17, provides additional support for an ischemic mechanism of acute nerve dysfunction.

Short-Term Effects of Nerve Compression (Effects within Days)
Com- pression of 4.0 kilopascals led to an elevated endoneu- rial pressure, which persisted for twenty-four hours after release of the cuff. Furthermore, the endoneurial pres- sures at twenty-four hours after release of the cuff increased with increasing durations of compression. His- tological examination demonstrated endoneurial edema in the nerves that had been subjected to eight hours of compression but not in those subjected to shorter dura- tions. Eight hours of compression led to an increase of the endoneurial pressures to levels that can reduce in- traneural blood flow51.

The study demonstrated that, af- ter low elevations of extraneural pressure for only two hours, endoneurial fluid pressures increased rapidly and the increases persisted for at least an additional twentyfour hours40. These effects probably are due to the in- creased vascular permeability of the epineurial and en- doneurial vessels after compression. Other studies have demonstrated that ischemia alters the structure of the endothelial and basement membranes over a similar time-frame2.

Long-Term Effects of Nerve Compression (Effects within Weeks)
Edema was visible in the sub- perineurial space within four hours in all compression subgroups, and it persisted for the entire duration of the study. Inflammation and fibrin deposits occurred within hours after compression, followed by prolifera- tion of endoneurial fibroblasts and capillary endothe- lial cells. Vigorous proliferation of fibrous tissue was noted within days, and marked fibrosis and sheets of fibrous tissue were seen extending to adjacent structures at twenty-eight days. Endoneurial invasion of mast cells and macrophages was noted, especially at twenty-eight days. Axonal degeneration was noted in the nerves sub- jected to 10.7 kilopascals of compression and, to a lesser extent, in those subjected to 4.0 kilopascals of compres- sion. It rarely was seen in the nerves subjected to 1.3 kilopascals of compression. Axonal degeneration was associated with the degree of endoneurial edema. De- myelination and Schwann-cell necrosis at seven and ten days was followed by remyelination at fourteen and twenty-eight days. Demyelination was prominent in the nerves subjected to 4.0 kilopascals of compres- sion and, to a lesser extent, in those subjected to1.3 kilo- pascals of compression.

The tension of the ligatures or the inner diameter of the tube generally was selected so that blood flow was not visibly restricted. The re- sponse of nerves to compression in these studies was similar to that in the experiments involving compression with a cuff. For example, the application of loose liga- tures around the sciatic nerve led to perineurial edema with proliferation of endothelial cells and demyelina- tion within the first few days, to proliferation of fibro- blasts and macrophages as well as degeneration of distal nerve fibers and the beginning of nerve sprouts within one week, to invasion by fibrous tissue and remyelina- tion at two weeks, to regeneration of nerve fibers as well as thickening of the perineurium and the vessel walls at six weeks, and to remyelination of distal nerve segments at twelve weeks73.

Applica- tion of silicone tubes with a wide internal diameter can induce increased expression of interleukin-1 and trans- forming growth factor beta-1 in the nerve cell bodies in the dorsal root ganglia, but the relevance of this finding remains to be clarified92. The limitations of these models are that (1) the effects of the tissue inflammatory reac- tion to the device (foreign-body reaction) usually are not considered but do occur29 and (2) it is not possible to measure or control the applied extraneural pressure. However, these observational studies provide some in- sight into the biological response of the nerve to chronic low-grade compression.

In a few case reports on patients in whom a nerve segment was resected, the nerve at the site of the injury was compared with a nerve at a site proximal or distal to the injury47,55,82. In each instance, there was thickening of the walls of the microvessels in the endo- neurium and perineurium as well as epineurial and peri- neurial edema, thickening, and fibrosis at the site of the injury. Thinning of the myelin also was noted, along with evidence of degeneration and regeneration of fibers. The patients in these reports had advanced stages of compression syndrome. Earlier in the course of the dis- ease, a segment of the nerve usually is compressed with disturbance of the microcirculation, which is restored immediately after transection of the flexor retinaculum. There is usually both an immediate and a delayed return of nerve function, indicating the importance of ischemia in the early stages of compression syndrome43.

The tissues that lie next to a nerve, within a confined space (for example, synovial tissue within the carpal tunnel), are more easily obtained and can provide infor- mation on the response of these tissues to compres- sion18,20,32,53,61,69,70,91.
The im- portant findings were increased edema and vascular sclerosis (endothelial thickening) in samples from the patients, who were between the ages of nineteen and seventy-nine years. Inflammatory cell infiltrates (lym- phocytes and histiocytes) were observed in only 10 per- cent (seventeen) of the 177 samples. Surprisingly, the prevalence of fibrosis (3 percent [five of 177]) was much lower than the prevalences of 33 percent (fifteen of forty-five) to 100 percent (twenty-one of twenty-one) reported in the other studies.

The initial symptoms of compres- sion of the median nerve at the wrist (carpal tunnel syndrome) usually are intermittent paresthesia and def- icits of sensation that occur primarily at night (stage I). These symptoms probably are due to changes in the intraneural microcirculation that are associated with some edema, which disappears during the day.
Progres- sive compression leads to more severe and constant symptoms that do not disappear during the day (stage II); these include paresthesia and numbness, impaired dexterity, and, possibly, muscle weakness. During this stage, the microcirculation may be altered throughout the day by edema and there may be morphological changes such as segmental demyelination.
In the final stage (stage III), there are more pronounced morpho- logical changes accompanied by degeneration of the nerve fibers; these changes manifest as constant pain with atrophy of the median-nerve-innervated thenar muscles and permanent sensory dysfunction.

In a study of the ulnar nerve at the elbow, localized areas of strain (nerve-stretching) of greater than 10 percent were observed in some cadav- eric arms83. A strain of 6 to 8 percent can limit blood flow in a nerve or can alter nerve function5,37,59.

Overview
First, elevated extraneural pressures can, within min- utes or hours, inhibit intraneural microvascular blood flow, axonal transport, and nerve function and also can cause endoneurial edema with increased intrafascicular pressure and displacement of myelin, in a dose-response manner. Pressures of 2.7 kilopascals (twenty millimeters of mercury) can limit epineurial blood flow, pressures of 4.0 kilopascals (thirty millimeters of mercury) can limit axonal transport and can cause nerve dysfunction and endoneurial edema, and pressures of 6.7 kilopascals (fifty millimeters of mercury) can alter the structure of myelin sheaths.

Second, on the basis of several animal models, it is apparent that low-magnitude, short-duration extraneu- ral pressure (for example, 4.0 kilopascals [thirty millime-
ters of mercury] applied for two hours) can initiate a process of nerve injury and repair and can cause struc- tural tissue changes that persist for at least one month.

The cascade of the bio- logical response to compression includes endoneurial edema, demyelination, inflammation, distal axonal de- generation, fibrosis, growth of new axons, remyelination, and thickening of the perineurium and endothelium. The degree of axonal degeneration is associated with the amount of endoneurial edema.

Third, in healthy people, non-neutral positions of the fingers, wrist, and forearm and loading of the fingertips can elevate extraneural pressure in the carpal tunnel in a dose-response manner. For example, fingertip pinch forces of five, ten, and fifteen newtons can elevate pres- sures to 4.0, 5.6, and 6.6 kilopascals

Fourth, in a rat model, exposure of the hindlimb to vibration for four to five hours per day for five days can cause intraneural edema, structural changes in my- elinated and unmyelinated fibers in the sciatic nerve, and functional changes both in nerve fibers and in non- neuronal cells.

Fifth, exposure to vibrating hand tools at work can lead to permanent nerve injury with structural neuronal changes in finger nerves as well as in the nerve trunks just proximal to the wrist. The relationships between the duration of exposure, the magnitude of the vibration, and structural changes in the nerve are unknown.

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Attenuation of Experimental Pain by Vibro-Tactile Stimulation in Patients with Chronic Local or Widespread Musculoskeletal Pain

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Viktig studie som nevner smertedempende effekt av høyfrekvent vibrasjon på huden. Det er A-beta fiber (pacini) som blir stimulert, som er de tettes og tykkest myeliniserte og raske nervefibrene. «homotopic» betyr «på samme sted». Med vibrasjon på samme sted som smerten får man en 40% smerteredusering, sier studien. Nevner også at smertereduksjonen kommer av spinal inhibition (gate control).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136545/

Several lines of evidence implicate abnormalities of central pain processing as contributors for chronic pain, including dysfunctional descending pain inhibition. One form of endogenous pain inhibition, diffuse noxious inhibitory controls (DNIC), has been found to be abnormal in some chronic pain patients and evidence exists for deficient spatial summation of pain, specifically in FM. Similar findings have been reported in patients with localized musculoskeletal pain (LMP) disorders, like neck and back pain.

Whereas DNIC reduces pain through activation of nociceptive afferents, vibro-tactile pain inhibition involves innocuous A-beta fiber.

Homotopic vibro-tactile stimulation resulted in 40% heat pain reductions in all subject groups.

Although the pathogenesis of CWP is only incompletely understood (Vierck, Jr. 2006), increasing evidence points toward the important roles of abnormal peripheral (Staud et al., 2009; Staud et al., 2010) and central pain mechanisms (Desmeules et al., 2003; Staud 2009). Biochemical abnormalities in the cerebrospinal fluid (CSF) of some CWP patients, like FM include low levels of serotonin (5HT) and noradrenaline (NA) (Russell et al., 1992), high levels of substance P (Russell et al., 1994; Vaeroy et al., 1988) and of nerve growth factors (Giovengo et al., 1999) providing indirect evidence for abnormal central pain modulation. Abnormal levels of CSF neurotransmitters may also account for some of the symptoms experienced by many CWP patients such as sleep disturbance, fatigue, cognitive abnormalities, and depression. Moreover, reductions of 5HT and NA in the CSF seem to suggest dysfunction of the descending inhibitory systems (Lautenbacher and Rollman 1997) which may, at least in part, be responsible for the widespread pain of these patients.

Inadequate pain inhibition has been detected in FM patients but not in healthy control subjects (NC) during noxious counter-stimulation experiments (Kosek and Hansson 1997; Lautenbacher and Rollman 1997; de Souza et al., 2009). Similar findings have been reported in patients with localized musculoskeletal pain (LMP) disorders like osteoarthritis (OA) (Arendt-Nielsen et al., 2010). Dysfunctional central pain inhibition also appears to be responsible for abnormal spatial summation (Julien et al., 2005) and reduced pain habituation in FM patients (Montoya et al., 2006; Smith et al., 2008).

A mechanism yet to be tested is that of vibro-tactile analgesia which relies on high frequency stimulation of low threshold A-beta mechanoreceptors (e.g., Pacinian corpuscles), segmental dorsal horn mechanisms (Salter and Henry 1990a; Salter and Henry 1990b), and possibly mechanisms within the somatosensory cortex (Peltz et al., 2011) (Tommerdahl et al., 1999a; Tommerdahl et al., 2005).

Vibro-tactile analgesia is mechanistically very different from various forms of counter-stimulation that rely on stimulation of high threshold primary afferent neurons (e.g., DNIC and high intensity- low frequency TENS). Vibro-tactile stimulation of A-beta primary afferents produces potent inhibition of dorsal horn nociceptive neurons (Salter and Henry 1990a; Salter and Henry 1990b) and somatosensory cortical neurons in area 3B (Tommerdahl et al., 1999a).

verage (SD) vibration intensity at detection threshold was .012 (.006) m/s2 for NC, .013 (.004) m/s2 for FM, and .013 (.004) m/s2 for LMP participants.

The results of our study demonstrate robust attenuation of experimental pain by either homotopic or heterotopic vibro-tactile stimulation in NC, FM, and LMP patients. The magnitude of endogenous analgesic effects was large (ca. 40% pain reductions) and not statistically different across all three subject groups.

The analgesic effect of vibro-tactile stimuli was greater during homotopic compared to heterotopic conditioning stimulation (40% vs. 32%) in all groups studied. Considerable neurophysiological evidence supports spinal segmental inhibition as an explanation for this effect (Salter and Henry 1990a; Salter and Henry 1990b). Such an analgesic mechanism had originally been envisioned by Melzack & Wall in 1965 (Melzack and Wall 1965).

Overall, vibro-tactile stimulation appears to reliably activate analgesic mechanisms in chronic musculoskeletal pain patients which can powerfully inhibit experimental pain.

A major component of vibro-tactile analgesia is likely related to A-beta mediated afferent inhibition of dorsal horn nociceptive neurons (Salter and Henry 1990a; Salter and Henry 1990b).

Using optical intrinsic signal imaging, Tommerdahl and Whitsel have shown that cutaneous vibro-tactile stimuli result in frequency-dependent reduction in cortical responsiveness to heat nociceptive input. (Whitsel et al., 1999; Tommerdahl et al., 1999b). In contrast to 25 Hz skin stimulation which does not seem to change S1 activation, vibro-tactile stimulation frequencies, similar to those used in the present study (100 Hz), resulted in potent suppression/inhibition of heat nociceptive responses within S1 (Tommerdahl et al., 1999a; Whitsel et al., 2000).

Recent evidence indicates that patients with idiopathic pain disorders, such as temporo-mandibular disorders, FM, tension headache, migraine and irritable bowel syndrome, demonstrate lower DNIC efficiency compared to NC (Julien et al., 2005; Maixner et al., 1995; Pielsticker et al., 2005). Similarly, less efficient DNIC has been associated with an extended history of pain among healthy subjects (Edwards et al., 2003).

Overall, vibro-tactile stimulation tests appear to be well tolerated by study participants and well suited for characterizing not only pain modulatory capacities of NC but also of individuals with chronic pain.

Given the potent effects observed in the present study, clinical investigations of analgesia using vibro-tactile stimulation in various musculoskeletal pain disorders, including FM and LMP, seem warranted.

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Effects of Respiratory-Muscle Exercise on Spinal Curvature

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Nevner hvor mye diafragma og pustemuskler har å si for kontroll og stabilitet i bevegelse. Bla. kjernemuskulatur og intraabdominalt trykk.

http://posturalrestoration.com/media/pdfs/Effects_of_Respiratory-Muscle_Exercise_on_Spinal_Curvature.pdf

Respiratory-muscle exercises are used not only in the rehabilitation of patients with respiratory disease but also in endurance training for ath- letes. Respiration involves the back and abdominal muscles. These muscles are 1 of the elements responsible for posture control, which is integral to injury prevention and physical performance.

The results suggest that respiratory-muscle exercise straightened the spine, leading to good posture control, pos- sibly because of contraction of abdominal muscles.

In competitive sports, the spine of young athletes can have excess thoracic kyphosis and lumbar lordosis because it is the conduit for transferring mechanical power between the upper and lower extremities during rapid and forceful movements.1

Under the influence of these forces, athletes have much degeneration of the intervertebral disks,2 and the loss of disk height with denaturation is associated with increased spine curva- ture.1 Thoracic kyphosis and lumbar lordosis contribute to back pain.3

The loss or increase of lumbar lordosis correlates well with the incidence of chronic low back pain.4,5 In addition, thoracic kyphosis leads to shoulder pain.3

Spinal-alignment control is essential for preventing various injuries. Align- ment depends on muscle strength and balance, muscle tightness, and skeletal structure.9

The trunk muscles are grouped into 2 categories: global and local stabilizers.10 The global stabilizers com- prise superficial muscles such as the rectus abdominis and longissimus muscles, and the local stabilizers are deep muscles, for example, the transverse abdominal and multifidus muscles.10 Cholewicki et al11 reported that thecontraction of local stabilizers is indispensable to trunk stability; that is, the trunk becomes unstable in the case of contraction of global stabilizers alone. The unstable trunk increases stress to the ligament and bone that control the end of motion and cause pain such as back pain.12

Respiratory-muscle exercises are used in the reha- bilitation of chronic obstructive pulmonary disease18 and endurance exercise for athletes.19 The muscles comprise the diaphragm, intercostal muscles, and the accessory muscles of respiration.20 The accessory muscles of res- piration consist of several of the trunk muscles, includ- ing local stabilizers. Therefore, this study focused on exercises for the respiratory muscles, which have the advantage that the load can be accurately set by regulating frequency and depth of breathing.

Increased spine curvature is responsible for low back pain4,5 and swim- mer’s shoulder,6 so respiratory-muscle exercise may prevent these dysfunctions.

Because muscle strength for trunk flexion was noted to increase only in the exercise group, we conclude that the exercises strongly affected the abdominal muscles. Abe et al32 reported that the transverse abdominal muscle is the most powerful in the abdominal muscle group with respect to respiration. The transverse abdominal muscle may have been specifically targeted in this exercise. This important muscle is a key local stabilizer.

Contraction of the transverse abdominis increases intra-abdominal pressure, which leads to lumbar
straightening.33 In addition, a rise in intra-abdominal pres- sure presses the rib cage upward and effectively allows the extension of the thoracic vertebrae.34

In addition, we attribute the decrease of thoracic curvatures to a stretching effect on the thorax. In a previous study, Izumizaki et al35 reported that thoracic capacity and rib-cage movement were changed by thixotropy, which is the exercise of maxi- mal expiration from maximum inspiration. The stiffness of the rib cage leads to thoracic kyphosis.3 In this study, repetitive deep breathing resolved the stiffness of the rib cage and straightened thoracic kyphosis. This process may be responsible for altering the spinal curvature.

These training methods require a long period of 12 weeks for improvement. By contrast, our intervention period was 4 weeks, so spinal alignment may be improved in a much shorter period.

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Diaphragm Postural Function Analysis Using Magnetic Resonance Imaging

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Studie som bekrefter alt om diafragma og dens bevegelse. Bl.a. at den har mye mev holdning og bevegelse å gjøre, og at baksiden beveger seg mest. Nevner også hva som er optimal bevegelse av diafragma for best fungere som stabilisator av ryggraden i bevegelse.

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0056724

When a load was applied to the lower limbs, the pathological subjects were mostly not able to maintain the respiratory diaphragm function, which was lowered significantly. Subjects from the control group showed more stable parameters of both respiratory and postural function. Our findings consistently affirmed worse muscle cooperation in the low back pain population subgroup

The diaphragm and deep stabilization muscles of the body have been described as an important functional unit for dynamic spinal stabilization [1], [2]. The diaphragm precedes any movement of the body by lowering and subsequently establishing abdominal pressure which helps to stabilize the lumbar part of the spine. Proper activation of the diaphragm within the stabilization mechanism requires the lower ribs to be in an expiratory (low) position. During the breathing cycle, the lower ribs have to stay in the expiratory position and only expand to the sides. This is an important assumption for the straight and stabilized spine. Under these conditions, the motion of the diaphragm during respiration is smooth, and properly helps to maintain abdominal pressure.

Dysfunction of the cooperation among diaphragm, abdominal muscles, pelvic floor muscles and the deep back muscles is the main cause of vertebrogenic diseases and structural spine findings such as hernia, spondylosis and spondylarthrosis [3], [4].

Noen studier å se nærmere på her:
Studies focused on diaphragm activation with the aim of posture stabilization include Hodges[11]–[14], who concluded phase modulation corresponding to the movement of the upper limbs in diaphragm electromyography records. Some works deal with various modes of diaphragm functions in various respiration types [15], [16] or in situations not directly related to respiration, e.g. activation during breath holding [17]. These studies have always concentrated on healthy subjects who did not exhibit symptoms of respiratory disease or vertebrogenic problems.

Og enda fler å se nærmere på her, spesielt relatert til scoliose:
Gierada [20] also used MRI for observing the anteroposterior size of the thorax, the height of the diaphragm during inspiration and expiration, and also the ventral and dorsal costophrenic angle during maximal breathe in and out. Kotani[21] and Chu [22] assessed chest and diaphragm movements for scoliosis patients. Suga [23]compared healthy subjects and subjects with chronic obstructive pulmonary disease (COPD), measuring the height, excursions and antero-posterior (AP) size of the diaphragm with the zone of apposition. Paradox diaphragm movements for subjects with COPD were investigated by Iwasawa [10]. Iwasawa used deep breath sequences while comparing diaphragm height and costophrenic angles. The study consisted of healthy subjects and subjects with scoliosis. Kotani [21] concluded that there was ordinary diaphragm motion with limited rib cage motion in the scoliosis group. The position of the diaphragm was measured relative to the apex of the lungs to the highest point of the diaphragm. Chu [22] compared healthy subjects against subjects with scoliosis, finding the same amount of diaphragm movement for both groups. The scoliosis group had the diaphragm significantly lower in the trunk and relatively smaller lung volumes. The distance between the apex of the lungs and the diaphragm ligaments was measured by Kondo [24], comparing young and old subjects. The effect of intraabdominal pressure on the lumbar part of the spine was observed by MRI and pressure measurement by Daggfeldt and Thorstensson [25]. Differences in diaphragm movement while performing thoracic or pulmonary breathing with the same spirometric parameters were tested by Plathow[26]. Plathow also examined the vital capacity of the lungs compared with 2D and 3D views in[27]. He concluded that there was a better correlation between the lung capacity and the 3D scans. In another study, Plathow focused on dynamic MRI. He proved significant correlations among diaphragm length and spirometric values vital capacity (VC), forced expiratory volume (FEV1) and other lung parameters [28].

Nevner også hvordan MRI-funn i ryggraden ikke har noe med smerte å gjøre:
Jensen found no direct connection between certain types of structural changes and LBP. The only structural change related to pain was disk protrusion. Carragee [31] studied MRI findings of 200 subjects after a period of low LBP, and found no direct significant MRI finding related to low back pain.

Nevner at problemer med pustefunksjon kan være en større indikator på ryggsmerter enn forandringer i ryggsøylen:
The way in which the diaphragm is used for non-breathing purposes is affected by it’s recruitment for respiration [32]. There is evidence that the presence of respiratory disease is a stronger predictor for low back pain than other established factors [33]. However, the relationship between the respiratory function and the postural function is widely disregarded[34]. Body muscles coordination for posture stabilization is a complex issue, and the role of the diaphragm in this cooperation has not been intensively studied [35].

Målet med studien:
he main goal is to separate respiratory diaphragm movements from non-respiratory diaphragm movements, and then to evaluate their role in body stabilization.
We investigated diaphragm reactability and movement during tidal breathing and breathing while a load was applied to the lower limbs.

Eksempel på diafragmas bevegelse:

Viser normal(C2) reaksjon på aktivitet(S2) og forskjellen i unormal(C1) reaksjon ved rygglager:

Figure 4. Dif-curves (solid line) and extracted res-curves (red dashed line) and pos-curves (green dotted line).

Example of harmonic breathing (A), breath with a strong postural part after the load occurred (B), harmonic breath which became partly non-harmonic after the load occurred (C, D), and breath which almost lost its ability of respiration movement ability after the load occurred (E, F).

Om hvor mye diafragma beveger seg:

As in the case of respiratory frequency, there was no change in respiratory curve amplitude in the control group when a load was applied to the lower limbs (1823 journal.pone.0056724.e253&representation=PNG journal.pone.0056724.e254&representation=PNG, 1928 journal.pone.0056724.e255&representation=PNG journal.pone.0056724.e256&representation=PNG). By contrast, the pathological group showed lowered excursions when load was applied (870 journal.pone.0056724.e257&representation=PNG journal.pone.0056724.e258&representation=PNG, 540 journal.pone.0056724.e259&representation=PNG journal.pone.0056724.e260&representation=PNG). The inter-situational difference was significantly different amongst the groups with journal.pone.0056724.e261&representation=PNG. In comparison with the pathological group, the control group had 3 times bigger excursions in situation journal.pone.0056724.e262&representation=PNG, and 6.5 times bigger excursions in the situation journal.pone.0056724.e263&representation=PNG.

In addition, the measurements showed great motion of the posterior diaphragm part than of the anterior part. Injournal.pone.0056724.e266&representation=PNG, the antero-posterior ratio was journal.pone.0056724.e267&representation=PNG within the control group and journal.pone.0056724.e268&representation=PNG within the pathological group. In journal.pone.0056724.e269&representation=PNG, the control group raised the range of the posterior part to journal.pone.0056724.e270&representation=PNG mm, resulting in an antero-posterior ratio of journal.pone.0056724.e271&representation=PNG. The pathological group, by contrast, raised the range in the anterior area and reduced the range in posterior area, resulting in an antero-posterior ratio of journal.pone.0056724.e272&representation=PNG.

Om hvordan pusten reagererer annerledes ved ryggsmerter:

We concluded that there was slower and deeper respiratory motion (parameters journal.pone.0056724.e362&representation=PNG) for both observed situations. In addition, after the postural demands rose in situation journal.pone.0056724.e363&representation=PNG, the breathing speed increased significantly (journal.pone.0056724.e364&representation=PNG) in the pathological group. In the same manner the breath depth (journal.pone.0056724.e365&representation=PNG) lessened significantly (journal.pone.0056724.e366&representation=PNG) in the pathological group. There were bigger postural moves in the control group, and they remained bigger in both situations, rising equally for each group.

Ved ryggsmerter er diafragma høyere opp i kroppen og lungene blir mindre:

The inclination of the diaphragm was greater (i.e. it was more verticalized) in the control group. The pathological group had the diaphragm placed significantly higher in the trunk, as indicated by the journal.pone.0056724.e372&representation=PNG parameter.

Om forholdet mellom diafragma og smerte, hd er høyden på diafragma, jo høyere jo mer smerte:

Diaphragm height were the only diaphragm parameter which was statistically significantly correlated (p = 0.0035) with the subjects’ low back pain indicated during the month before imaging. Pearson correlation coefficient was 0.67.

Om hvor mye diafragma beveger seg:
In the results section, we concluded that there is a statistically significant difference in the range of motion (ROM) of the diaphragm. A two and three times greater ROM was noted in the control group, than in the pathological group in situations journal.pone.0056724.e379&representation=PNG and journal.pone.0056724.e380&representation=PNG. In addition, the average diaphragm excursions journal.pone.0056724.e381&representation=PNG (central part) in situation journal.pone.0056724.e382&representation=PNG were journal.pone.0056724.e383&representation=PNG mm in the control group and journal.pone.0056724.e384&representation=PNGmm in the pathological group. In situation journal.pone.0056724.e385&representation=PNG, journal.pone.0056724.e386&representation=PNG was journal.pone.0056724.e387&representation=PNG mm in the control group and journal.pone.0056724.e388&representation=PNG mm in the pathological group.

We observed that the diaphragm was significantly higher for the pathological group. This may be a mechanism by which the pathological group was able to keep the diaphragm excursions more evenly spread after the postural demands increased.

Diafragma beveger seg normalt mer på baksiden:
We also observed that the diaphragm was more contracted in the posterior part for the control group. Diaphragm inclination measurements showed significant lowering of the posterior part of the diaphragm relative to the anterior part of the diaphragm for the control group. The pathological group kept the diaphragm in a more horizontal position.

Suwatanapongched [43]concluded that there was flattening of the diaphragm in the older population in his study. Our results did not show any significant age-related correlation of diaphragm flatness. Instead, the only significant correlation that we observed was between diaphragm height and the LBP intensity of the pathological group during the month before the measurements were made.

Jo høyere opp diafragma er, jo vanskeligerere blir den å bevege:
We assume that this diaphragm bulging is due to worse ability to contract the diaphragm properly. To the best of our knowledge, there are no results in the literature for measurements of diaphragm flatness in subjects suffering from LBP. Worse ability to contract the diaphragm in the pathological group is also supported by the significantly higher position in the trunk.

No correlation was concluded between measured parameters and pain intensity except for bulging (i.e. long term pain) of the diaphragm, as was discussed above. The results indicate that, as the pain is long term, the patients do not change their respiratory patterns according to fluctuations in the chronic LBP.

The significant differences in the harmonicity of the diaphragm motion observed in this study indicate changes in the central nervous system related to diaphragm function in subjects with pathological spinal findings suffering from various intensities of chronic low back pain. Low back pain is a wide-spread and widely studied phenomenon. Alternating respiratory patterns and anatomical changes in the diaphragm have been assessed in LBP subjects. Studies concluding increased susceptibility to pain and injury [1], [13], [49] identified differences in muscle recruitment in people suffering from LBP. Janssens [50] used fatigue of inspiratory muscles, and observed altered postural stabilizing strategy in healthy subjects. Jenssens also observed non-worsening stabilization with an already altered stabilizing strategy in subjects suffering from LBP. Grimstone [51] measured respiration-related body imbalance in subjects suffering from LBP, observing worse stability in subjects with LBP. Kolar [44] investigated differences in diaphragm contractions between healthy subjects and LBP subjects. He observed lesser contractions in the posterior part of the diaphragm while the postural demands on the lower limbs increased, and he suspected that intra-abdominal pressure lowering might be the underlying mechanism of LBP. Roussel [34] assessed the altered breathing patterns of LBP subjects during lumbopelvic motor control tests, concluding that some subjects used an altered breathing pattern to provide stronger support for spinal stability.
In our measurements, we did not observe the same diaphragm excursions in the posterior part of the diaphragm for healthy subjects and for subjects suffering from LBP as were observed by[44]. The excursions were reduced in the pathological group. In contrast with Kolar’s findings[44], we concluded that there was also lowering of the diaphragm inspiratory position in the pathological group in situation journal.pone.0056724.e399&representation=PNG. Our measurements support the hypothesis of less diaphragm contraction in the pathological group, with a significant correlation between diaphragm bulging and the intensity of the patient’s low back pain.

Om hvordan magemuskler er nødvendig for diafragma stabilitet:
In the pathological group, the abdominal muscles lack the ability to hold the ribs in lower position. For this reason, the insertion parts of the diaphragm are not fixed and the diaphragm muscle changes its activation. The diaphragm is disharmonic in its motion, which causes problems with providing respiration and at the same time retaining abdominal pressure. The muscle principle for spine stabilization is therefore violated, and is replaced by a substitute model, which tends more easily toward the emergence of low back pain, spine degeneration or disc hernia.

Reversed causation is always a possibility, i.e. it is possible that the diaphragm behavior is changed in order to stabilize the spine after the deep intrinsic spinal muscles fail. During these changes, breathing patterns may occur, e.g. breath holding and decreased diaphragm excursions.

Our study shows a way to compare the diaphragm motion within the group of controls without spinal findings and those who have a structural spinal finding, e.g. a hernia, etc., not caused by an injury. In this way, we confirm our experience of the influence of the diaphragm on spinal stability and respiration. The control group show a bigger range of diaphragm motion with lower breathing frequency. The diaphragm also performs better harmonicity (coordination) within its movement. The postural and breathing components are better balanced. This fact is very important for maintaining the intraabdominal pressure, which helps to support the spine from the front. For this reason, it plays a key role in treating back pain, hernias, etc. In the group of controls we also found a lower position of the diaphragm while it was in inspiration position in tidal breathing and also while being loaded. These facts also support the ability of the diaphragm to play a key role in maintaining the good stability of the trunk. It is also important that we are able to separate the phases of diaphragm movement. This supports both the postural function and the breathing function of this muscle due to MR imaging.

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Pain Sensitivity and Analgesic Effects of Mindful States in Zen Meditators: A Cross-Sectional Study

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Nevner hvordan smerteopplevelse blir mindre med meditasjon, men viser også til at det sannsynligvis er pustefrekvensen som gir den smertestillende effekten. Pluss den nevner hvordan frontallappen bidrar med smertestillende opioider.

http://www.psychosomaticmedicine.org/content/71/1/106.long

These results indicated that Zen meditators have lower pain sensitivity and experience analgesic effects during mindful states. Results may reflect cognitive/self-regulatory skills related to the concept of mindfulness and/or altered respiratory patterns.

Mindfulness can be described as an equanimous state of observation of one’s own immediate and ongoing experience.

Mindfulness has been described as “intentional self-regulation of attention from moment to moment … of a constantly changing field of objects … to include, ultimately, all physical and mental events….” (5). Furthermore, an attitude of acceptance toward any and all experience is stressed. Traditional accounts of mental and emotional transformation accompanying mindful practice (6,7) are supported by scientific findings of psychological and biological effects on practitioners (8–10) and patients (5,11–15).

Mindfulness-based therapies have reported success treating anxiety (11,15), obsessive compulsive disorder (13), and depression (12,14). Positive correlations between meditation experience of Buddhist monks and positive affect (10) have been reported. Increases in positive affect have also been observed in a longitudinal study in which naïve subjects were trained to meditate (8).

It is well known that cognitive manipulations, such as hypnosis, attention, expectancy or placebo, can influence the experience of pain and the associated neurophysiological activity (17–19). There is also mounting evidence that mindfulness may be effective in treating chronic pain.

Significant positive improvements were found on all measures immediately after the 10-week training program. However, follow-up evaluation showed stable improvements on most measures with the exception of present moment pain. The authors interpreted the results as the acquisition of an effective coping strategy for pain, where the pain itself did not change but the relation or stance taken toward the pain was positively altered.

Changes in pain were further examined in relationship to meditation training. The amount of meditation experience of individual practitioners predicted the degree of pain intensity modulation (i.e., versus baseline) with more hours of experience leading to greater reductions in pain intensity during the mindfulness condition [r(9) = −.82, p< .01].

Notably, pain modulation induced by mindfulness (relative to baseline-1) was correlated with the corresponding changes in respiratory rate across all subjects [intensity: r(23) = .37, p = .03; unpleasantness: r(23) = .42, p = .02]. Furthermore, the significant decrease in pain intensity reported above in the meditators during the mindfulness condition relative to baseline-1 (Figure 2) did not reach significance after including the changes in respiration as a covariate [F(1,11) = 3.02, p = .11]. In contrast, the significant increase in pain intensity reported by the control subjects in the concentration condition remained significant after accounting for changes in respiratory rates [F(1,11) = 20.94, p = .001]. These effects suggest that the changes in pain induced by mindfulness, but not concentration, may be at least partly accounted for by changes in respiration.

The main findings are the following:

  • 1) Meditators required hotter temperatures than controls to experience moderate pain.
  • 2) As hypothesized, meditators experienced less pain while attending mindfully, whereas control subjects did not show such modulation.
  • 3) Unexpectedly, analgesic effects of mindfulness were more clear on the sensory dimension of pain (i.e., perceived intensity) than the affective dimension of pain (i.e., pain unpleasantness), although effects were observed in the same direction.
  • 4) The magnitude of the analgesic effect of mindfulness was predicted by the number of hours of meditation practice in meditators.
  • 5) When attention was directed toward the stimulation, with no mention of attending mindfully, control subjects showed the expected increase in pain intensity and unpleasantness whereas meditators did not differ from baseline.
  • 6) Physiologically, meditators had slower breathing rates than controls, consistent with their self-assessed reduced reactivity. Importantly, changes in respiratory rate predicted the changes in felt pain and the analgesic effect of mindfulness states was no longer significant after accounting for changes in respiratory rates (covariance).
  • 7) On a mindfulness scale, meditators scored higher on the tendency to be observant and nonreactive. Higher scores on these dimensions of mindfulness were further associated with lower pain sensitivity and slower respiratory rates.

Zen meditation was associated with lower pain sensitivity as demonstrated by the higher temperatures required to produce moderate pain. The observed difference (49.9°C versus 48.2°C) should be considered large as it typically corresponds to an increase of about 50% on a ratio scale of pain perception or 20 to 25 points on a 0 to 100 numerical pain scale, based on similar psychophysical methods (28,33).

While attending mindfully, the Zen practitioners showed reductions of 18% pain intensity. Remarkably, individuals with more extensive training experienced greater reduction in pain. This finding is extremely important as it suggests that the observed pain reduction may not simply reflect a predisposition to meditation (individual differences) but may also involve experience-dependent changes associated with practice. This is in line with other studies linking meditation training with mindfulness, medical symptoms, and well-being (16); attention performance, anxiety, depression, anger, cortisol and immunoreactivity (34); an inverted U-shaped function of attention-related brain activity (35); electrophysiological markers of positive affect (10); positive affect and stronger immune responses (8); and cortical thickness and gray matter density (9,36,37).

The analgesic effects of mindful attention may relate to the physiological state induced as suggested by the respiration data. Overall, the meditators breathed at a slower rate than control subjects in all conditions and their mean respiratory pattern followed that of their pain ratings. In contrast, respiratory rate did not change noticeably across conditions in the control subjects. Slower breathing rates (typically meditators) were associated with less reactivity and with lower pain sensitivity. These relationships suggested that the meditators were in a more relaxed, nonreactive physiological state throughout the study, which culminated in the mindfulness condition and which influenced the degree to which they experienced pain.

The covariance analysis suggested that this analgesic effect could be mediated at least in part by the observed change in respiration.

A neuro-chemical model of meditation put forth by Newberg and Iversen (47) offers a possible explanation for our results. Meditation practice, involving volitional regulation of attention, seems to activate prefrontal cortex (35,48,49); this has been observed during Zen practice (50). Increases in prefrontal activation can stimulate the production of b-endorphin (e.g., in the arcuate nucleus of the hypothalamus) (47). B-endorphin is an opiate associated with both analgesia and a reduction in respiratory rate as well as decreases in fear and increases in joy and euphoria (47). Interestingly, the direction of attention toward breathing and the volitional control of breathing rates are part of many meditative techniques; however, causation can obviously not be inferred from those observations.

Another related possibility is that meditation leads to reductions in stress and stress-related chemicals, such as cortisol which interact with the opiate system. A reduction of cortisol can greatly enhance the binding potential/efficacy of endogenous opioids (27), possibly contributing to a downregulation of nociceptive responses. Studies have reported evidence of reduced cortisol responses in meditators (34,52,53).

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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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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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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. «