Stikkordarkiv: bindevev

Physiopathology of intratendinous calcific deposition

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Kalsium ansamlinger i sener eller andre strukturer i bevegelsesapparatet kan bidra til smertetilstander. Denne studien går igjennom hvordan disse oppstår slik at vi kan få en bedre forståelse av hva vi kan gjøre med det. Store ansamlinger kan sees på røntgen, men man kan også ha mikroskopiske ansamlinger som bidrar til plager uten å være synling på røntgen.

Det er spesielt vanlig blant de med diabetes (30%) og assosieres ofte med tyroidea problemer eller andre hormonproblemer. Genetisk predisposisjon er også en viktig faktor.

Ofte starter det med en skade, hvor det så skjer en kursendring i helbredelsesprosessen som gjør at kalsiumavleiringer eller andre problemer fremtrer og bidrar til smerteproblematikk.

http://www.biomedcentral.com/1741-7015/10/95

In calcific tendinopathy (CT) calcium deposits in the substance of the tendon. CT is particularly common in the rotator cuff tendons (RCTs) and supraspinatus tendon, and Achilles tendon and patellar tendon. CT of the rotator cuff is common in Caucasian populations, with a reported prevalence of 2.7% to 22%, mostly affecting women between 30 and 50 years. The most frequently involved tendon is the supraspinatus tendon, and in 10% of patients the condition is bilateral (Figure 1) [1].

(kalsiumansamlinger vises ytterst og øverst på humerus)

(kalsiumansamling vises i ackillesenen)

Clinical manifestations of the calcific process within the tendons include chronic activity-related pain, tenderness, localized edema and various degrees of decreased range of motion (ROM). CT of the rotator cuff shows a tendency toward spontaneous resorption of the deposits and symptoms often resolve spontaneously, although some authors described persistent pain at long time follow-up and persistent reduction of ROM [5,6].

Microscopic calcifications which are not detectable at plain radiography can also occur in chronic tendinopathy. A histological study showed high incidence of small calcium deposits in tendinopathic supraspinatus tendons [8]. Microscopic calcium deposits are frequent also in diabetic patients [9].

Specimens of RCTs obtained during surgery consist of a gritty mass of sandy material or a toothpaste-like fluid, and the deposits were described as a white amorphous mass composed of many small round or ovoid bodies. Later, X-ray diffraction and infrared spectrometry and other techniques identified the material of calcific deposits as calcium carbonate apatite [18–20].

Uhthoff and coworkers hypothesized that a favorable environment permits an active process of cell-mediated calcification, usually followed by spontaneous phagocytic resorption [28]. They describe four stages in the calcifying process of the rotator cuff: precalcific phase, calcific phase, resorptive phase, and repair phase. All phases may occur concomitantly in the same tendon.

Finally, bone is deposited and the spur is formed. No inflammatory cells or microtears were identified. The authors believe that the increased surface at the tendon-bone junction may represent an adaptive mechanism to increased mechanical loads.

An association between CT and diabetes and thyroid disorders has been shown, but the precise mechanism is still unknown [1]. Patients with associated endocrine disorders present earlier onset of symptoms, longer natural history, and they undergo surgery more frequently compared to a control population [61,62]. More than 30% of patients with insulin-dependent diabetes have tendon calcification [63]. The exposure of proteins to high levels of sugar moieties cause the glycosylation of several extra-cellular matrix proteins, which can modify the extracellular matrix by cross-linking proteins.

Effectiveness of myofascial release: Systematic review of randomized controlled trials

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Denne viser til en økende grad av kvalitet på studier på myofascial release, som Strukturell Integrering er. Konklusjonen er at det er god evidens for å bruke dette mot mange muskel- og ledd smertetilstander, og at denne behandlingsformen faktisk kan konkurrere med andre behandlingsformer.

http://www.bodyworkmovementtherapies.com/article/S1360-8592(14)00086-2/fulltext

Seventeen studies were with higher methodological quality and the remaining 2 were of moderate quality, which is appreciable for a relatively new approach with considerable amount of practice variations.

The results of the studies were encouraging, particularly with the recently published studies. In many RCT’s the MFR was adjunctive to other treatments and the potential-specific MFR effect cannot be judged.

Nine studies concluded that MFR may be better than no treatment or sham treatment for various musculoskeletal and painful conditions. Seven studies demonstrated that MFR with a conventional therapy is more effective than a control group receiving no treatment (3 studies), sham treatment (1 study) or with a conventional therapy.

There is evidence that MFR alone or added to other conventional therapies, relieves pain and improves function not lesser than conventional therapies studied. According to these results, MFR may be useful as either a unique therapy or as an adjunct therapy to other established therapies for a variety of conditions like sub acute low back pain, fibromyalgia, lateral epicondylitis, plantar fasciitis, headache, fatigue in breast cancer, pelvic rotation, hamstring tightness etc.

Structure and Biomechanics of Peripheral Nerves: Nerve Responses to Physical Stresses and Implications for Physical Therapist Practice

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Nevner det aller meste om perifere nerver og hvordan de får plager av «normale» sitasjoner, som f.eks. musearm.

http://www.ncbi.nlm.nih.gov/pubmed/16386065

http://ptjournal.apta.org/content/86/1/92.long

Abstract

The structural organization of peripheral nerves enables them to function while tolerating and adapting to stresses placed upon them by postures and movements of the trunk, head, and limbs. They are exposed to combinations of tensile, shear, and compressive stresses that result in nerve excursion, strain, and transverse contraction. The purpose of this appraisal is to review the structural and biomechanical modifications seen in peripheral nerves exposed to various levels of physical stress. We have followed the primary tenet of the Physical Stress Theory presented by Mueller and Maluf (2002), specifically, that the level of physical stress placed upon biological tissue determines the adaptive response of the tissue. A thorough understanding of the biomechanical properties of normal and injured nerves and the stresses placed upon them in daily activities will help guide physical therapists in making diagnoses and decisions regarding interventions.

Figure 1.

Structural components of peripheral nerves. In the endoneurial compartment (En), a single Schwann cell envelops several unmyelinated axons, and another Schwann cell provides multiple wrappings of plasma membrane forming the myelin sheath of a myelinated axon. The portion of a myelinated axon myelinated by a single Schwann cell is called the internode, and internodes are separated by nodes of Ranvier. Schwann cells associated with both unmyelinated and myelinated axons are covered with a continuous basal lamina (BL). Capillaries (Cap) are present within the endoneurial compartment, and collagen fibers (Col) run primarily longitudinally between the axons. The axons, Schwann cells, collagen, and endoneurial fluid are bundled into a fascicle by the perineurium (Pe). The perineurium consists of several layers of flattened perineurial cells connected by tight junctions and covered internally and externally by a basal lamina. The layers of perineurial cells are separated by collagen fibers (Col) oriented obliquely. Several fascicles are bundled together by the epineurium (Ep) to form a nerve. The epineurium consists primarily of fibroblasts, collagen fibers (Col), and elastic fibers. The epineurium between fascicles is termed the interfascicular epineurium, and that encompassing all of the fascicles is termed the epifascicular epineurium. Arterioles (A) and veins are oriented primarily longitudinally within the epineurium.

Blood supply

The blood supply to nerves is provided by coiled segmental arteries that enter the epineurium periodically along the length of the nerve and form the vasa nervorum. Arteries divide into epineurial arterioles that form an anastomotic network running primarily longitudinally within the epifascicular epineurium and the interfascicular epineurium (Fig. 3). Epineurial arterioles are supplied with a perivascular plexus of serotoninergic, adrenergic, and peptidergic nerves.17,18 Perforating arterioles cross the perineurium at oblique angles and carry a short sleeve of perineurial cells into the fascicle.3,19 Perineurial arterioles have poorly developed smooth muscle and thus have limited ability to regulate intrafascicular blood flow.20 Within the endoneurium, arterioles immediately turn into large-diameter, longitudinally oriented capillaries that allow blood flow in either direction (Fig. 3).21 The endothelial cells of endoneurial capillaries are connected by tight junctions, thus forming the tight blood-nerve barrier.7 Venules return blood to the venous system. Of note, lymphatic capillaries are present only within the epineurium; there is no lymphatic drainage from the intrafascicular or endoneurial space.22

Biomechanical properties

Under normal physiological conditions imposed by posture and movement, nerves are exposed to various mechanical stresses. Stress is defined as force divided by the area over which it acts9,23–25 and can be applied to a nerve as tensile, compressive, or shear stress or as a combination of stresses (Fig. 4). Tensile stress may be applied to tissues either parallel or perpendicular to the length of the nerve, causing respective longitudinal or transverse stress in the nerve. When joint motion causes elongation of the nerve bed, the nerve is inherently placed under tensile stress and accommodates the stress by both elongating and gliding.15 The deformation or change in nerve length induced by longitudinal tensile stress is called strain and is expressed typically as percent elongation.23,26–28 Displacement or gliding of a nerve relative to the surrounding nerve bed is called excursion.29–31 The direction of excursion may be longitudinal or transverse, or both, relative to the nerve tract31,32 and is measured in millimeters.

Figure 4.

Physical stresses placed on peripheral nerve. Tensile stress applied longitudinally to peripheral nerve creates an elongation of the nerve (an increase in strain). The transverse contraction that occurs during this elongation is greatest at the middle of the section undergoing tensile stress.

When the nerve bed is elongated, the nerve is placed under increased tensile stress. With the elongation of the nerve bed, the nerve glides toward the moving joint,1,33,34 a movement termed convergence.1 Conversely, if the nerve bed tension is relieved during joint motion, the nerve will realign along the shortened nerve bed by gliding away from the moving joint, a movement termed divergence.33 Convergence in the median nerve may be demonstrated during elbow extension (Fig. 5). The motion elongates the bed of the median nerve, causing the nerve segment in the arm to glide distally toward the elbow and the nerve segment in the forearm to glide proxi mally toward the elbow. In contrast, elbow extension relieves the tensile stresses in the ulnar nerve bed, causing the ulnar nerve to diverge away from the elbow (Fig. 5).

Figure 5.

Excursion of the median nerve (solid line) and the ulnar nerve (dotted line) during elbow extension followed by wrist extension. The concepts of nerve convergence toward and divergence away from a moving joint are illustrated in measurements of excursion taken at each site indicated. All measurements are reported in millimeters of proximal (P) or distal (D) excursion. The direction of excursion is also represented by solid arrows for median nerve excursion and open arrows for ulnar nerve excursion. (A) With elbow extension from 90° of flexion to 0° of flexion, the median nerve bed lengthens and the median nerve glides toward the elbow (converges). With the same joint motion, the ulnar nerve bed shortens and the ulnar nerve glides away from the elbow (diverges). (B) With wrist extension from 0° of extension to 60° of extension, both nerve beds lengthen; thus, both nerves converge toward the wrist. The magnitude of excursion is greatest closest to the moving joint. Data were obtained from: aDilley et al,29 bWright et al,27 and cWright et al.33 Measurements of nerve excursion at the wrist and elbow in panel A were extrapolated from studies of nerve excursion during elbow flexion from 0° to 90°.27

Nerve Stiffness

First, a recent study43 measured greater nerve compliance in nerve segments that cross joints than in segments that do not cross joints.

Second, nerve stiffness is greater in long nerve sections and in nerve sections with numerous branches.15 Severing nerve branches or vessels but leaving the nerve in situ results in increased compliance and decreased stiffness.15

Third, nerve stiffness is greater when a nerve is elongated rapidly rather than slowly. In addition, the ultimate strain at the point of failure appears to be dependent on the rate of elongation.

When a nerve is placed under tension and maintained at that new fixed length over time, there is a reduction in the tension in the nerve or the force required to maintain the fixed length. The observed reduction in tension may be plotted in a stress-relaxation curve (Fig.8).25,44 The majority of relaxation occurs in the first 20 minutes of fixed elongation.25,44Stress relaxation in nerves that are stretched slowly is greater than in nerves that are stretched rapidly.25,37,44–46 This phenomenon was observed when comparisons were made for rabbit tibial nerves stretched at different rates to lengths 6% longer than their resting lengths. Over the 60-minute relaxation time, there was a 57% reduction in stress in nerves elongated at 0.08% per second,45 but only a 34% reduction in stress in nerves elongated at 3.0% per second.44

Figure 8.

Stress-relaxation curve demonstrating viscoelastic properties of peripheral nerve. When a nerve is elongated and the new length is kept constant, there is a rapid reduction in the stress within the nerve, expressed as percent reduced relaxation. Most of the relaxation occurs in the first 20 minutes. The degree of elongation affects the amount of stress relaxation that will occur. The dotted line represents a nerve that has been elongated to 6% above its resting length. The solid line represents nerves that have been elongated to 9% and 12% above their resting lengths. Greater stress relaxation was documented in nerves that underwent less elongation.25,44 Modified from Kwan MK, Wall EJ, Massie J, Garfin SR. Strain, stress, and stretch of peripheral nerve: rabbit experiments in vitro and in vivo. Acta Orthop Scand. 1992;63:267–272, with permission of Taylor and Francis AS.

However, a nerve stretched repetitively to 8% or 10% strain exhibits a reduced slope of the stress-strain curve, indicating that that nerve undergoes less stress with successive elongations because of increased compliance and decreased stiffness.

Compression of nerve

In addition to tensile stress, nerves are exposed statically and dynamically to compressive stresses. As mentioned previously, the laws of physics dictate that the cross-sectional area of a cylindrical object is reduced as the cylinder is elongated. As a nerve is elongated under tensile force, the nerve undergoes transverse contraction, which is resisted by the fluid and nerve tissue contained within the connective tissue sheath.15,39The magnitude of the transverse contraction stress is greatest at the center of the elongating segment15 (Fig. 4). Nerves also may be compressed externally by approximation to adjacent tissues, such as muscle, tendon, or bone, or by pressure increases in the extraneural environment. Compression of a nerve segment causes displacement of its internal contents in transverse and longitudinal directions. As shown in rat nerve, extraneural compression causes an immediate displacement of endoneurial fluid to the edges of a compressive cuff over 5 to 10 minutes and a much slower displacement of axonal cytoplasm over the course of hours.48 The damage to axons and myelin is greatest at the edges of the compressed zone,48,49 where the shear forces are highest.50

At the edges of the cuff, however, myelin retraction with resultant widening of nodes and paranodal demyelination occurred. These structural alterations in myelin may be expected to result minimally in impaired impulse conduction or maximally in demyelination and a conduction block.

In response to biomechanical stresses placed on a nerve as an individual assumes a posture or movement, the nerve follows the path of least resistance.29 Combinations of tensile, shear, and compressive stresses result in combinations of nerve excursion, strain, and transverse contraction. Because the biomechanical forces on the nerve are so intricately linked, the sequencing and range of joint movement affect the magnitude and direction of excursion,27,29 the magnitude of nerve strain,27,29,35 and the degree of transverse contraction at different sites along the nerve.27

Simultaneous nerve excursion, strain, and transverse contraction may be seen in the ulnar nerve as an example of responses to physical stresses imposed during movements of the upper limb. When the upper limb is maintained in a position of 90 degrees of shoulder abduction and 90 degrees of shoulder external rotation with the wrist neutral, and when the elbow is moved from 90 degrees of flexion to full extension, the ulnar nerve bed is shortened and the tensile stress on the nerve is decreased. With this motion, there is divergence of the ulnar nerve away from the elbow (Fig. 5), decreased nerve strain, especially at the elbow (Fig. 6), and decreased compression within the cubital tunnel.27,29,33 When the wrist then is extended from neutral to full extension, the ulnar nerve bed is lengthened, resulting in convergence of the nerve toward the wrist (Fig. 5), an increase in nerve strain (Fig. 6), and transverse contraction greatest in the nerve segment across the carpal bones and at the tunnel of Guyon.27,29,33 The magnitude of nerve strain and excursion will be greatest near the wrist, and the fascicles will rearrange as the nerve assumes a flattened oval shape. Because the nerve does not lie directly on the rotational axis of joint motion, the fascicles farthest from the axis will undergo greater strain than those closer to the center of rotation51

Figure 6.

Strain of the median nerve (solid line) and the ulnar nerve (dotted line) during elbow extension followed by wrist extension. Measurements at the sites indicated are reported as percent increase (↑) or percent decrease (↓) in strain. (A) With elbow extension from 90° of flexion to 0° of flexion, median nerve strain increases because of elongation of the nerve bed. Conversely, ulnar nerve strain decreases as the ulnar nerve bed shortens. (B) With wrist extension from 0° of extension to 60° of extension, the strain at the sites measured increases in both nerves as both nerve beds elongate. The magnitude of the strain is greatest closest to the moving joint. Data were obtained from: aWright et al27and bWright et al.33 Measurements of nerve excursion at the wrist and elbow in panel A were extrapolated from studies of nerve excursion during elbow flexion from 0° to 90°.27

Continuum of physical stress states

First, levels of physical stress lower than the levels required for tissue maintenance (low stress) result in a reduced ability of the tissue to tolerate subsequent stress and are consistent with tissue plasticity and response to functional demand.

Second, levels of physical stress in the range required for tissue maintenance (normal stress) result in no tissue adaptations and are considered to maintain a state of equilibrium.

Third, physical stress levels that exceed the range required for tissue maintenance (high stress) result in an increase in the tolerance of the tissue for stress in an effort to meet the mechanical demand.

Fourth, physical stress levels that exceed the capacity of some components of the tissue (excessive stress) result in tissue injury.

Fifth, levels of physical stress that are extreme (extreme stress) result in tissue death.

Finally, it is important to note that the physical stress level is a composite value with variable components of magnitude, time, and direction or type of stress.

 In the functional zone, the physical stresses on the nerve are sufficient to maintain a state of equilibrium and normal physiological function. In the dysfunctional zone, various levels of physical stress have altered the ability of the nerve to tolerate subsequent stress.

Figure 9.

Continuum of physical stress states. The white area represents the functional zone in which the physical stresses on the nerve are sufficient to maintain a state of equilibrium and normal physiological function. The shaded areas represent dysfunctional zones resulting from various levels of physical stress placed on the nerve tissue. Under conditions of prolonged low stress, the functional zone will shrink in width and shift to the left, reducing the ability of the tissue to tolerate subsequent stresses even of previously normal levels. Under conditions of high stress, the functional zone may expand and shift to the right, improving the ability of the tissue to tolerate subsequent physical stress. If the nerve is exposed to prolonged or repeated excessive stress, the functional zone will shrink in width. Although scarring of damaged tissue may enable the nerve to tolerate subsequent physical stresses, the physiological function of the nerve will be reduced. Exposure to extreme stress will result in disruption of axon continuity or neural cell death and significantly reduced physiological function.

Immobilization Stresses

Under conditions of immobilization, such as casting, splinting, and bracing, peripheral nerves are exposed to levels of physical stress that are lower than those necessary to maintain the nerves in a state of equilibrium or in a functional zone (Fig. 9). According to the Physical Stress Theory, nerve will undergo predictable physiological and structural modifications proportional to the levels of reduced stress and the duration of immobilization.2 Immobilization induces cell biological changes in axons and axon terminals52–54 and structural changes in myelin and nerve connective tissue layers that likely alter the ability of nerves to tolerate subsequent physical stress.

We hypothesize that after a period of immobilization, the width of the functional zone on the continuum of physical stress states will shrink and shift toward the left (Fig. 9).

Lengthening Stresses

Nerves are exposed to various levels of longitudinal tensile stress during limb-lengthening procedures, such as distraction osteogenesis (Ilizarov procedures), traction injuries, and stretching maneuvers. The tissue response is dependent upon the magnitude and duration of the tensile stress. The extant data indicate that lengthening of 6% to 8% for a short duration causes transient physiological changes that appear to be within the normal stress tolerance of the tissue, whereas acute strains of 11% and greater cause long-term damage and may be considered to be excessive or extreme stress states.

In cadavers, positioning in shoulder depression, 90 degrees of shoulder abduction, 90 degrees of shoulder external rotation, 70 degrees of forearm supination, 60 degrees of wrist extension, full finger extension, and full elbow extension resulted in 7.6%±8.2% (X̄±SD) strain in the median nerve measured just proximal to the wrist.28 Adults who were healthy and who were placed in this same position lacked 12±13 degrees (X̄±SD) of elbow extension because of substantial discomfort in the limb.61 The subjects reported pain of 5.1±1.9 (X̄±SD) on a 10-point visual analog scale, and 36% of the subjects reported paresthesia in the upper limb. Taken together, these findings suggest that many people are unable to tolerate levels of strain below the theoretical 11% threshold.

Compression Stresses

Compression on a nerve may be the result of extraneural force or may occur as transverse contraction secondary to increased longitudinal strain (Fig. 4). Compression stress of a low magnitude and a short duration may result in reversible physiological and minor structural changes. Compressive stress of a high magnitude, however, may result in structural alterations in myelin sheaths and even disruption of axons. Low-magnitude compressive stress applied over a long period of time may cause significant structural changes in the nerve secondary to impairment of blood flow and sequelae of ischemia.

As with strain-induced injury, a threshold for compression-induced nerve injury is difficult to determine. Common functional positions may result in compression pressures that approach or exceed the 20 to 30 mm Hg demonstrated to impair nerve blood flow.75 The carpal tunnel is a site well known for compressive damage to the median nerve and thus has been well studied. Carpal tunnel pressure in subjects who were healthy was measured at 3 to 5 mm Hg with the wrist in a neutral position.76–78 Simply placing the hand on a computer mouse was shown to increase the tunnel pressure from the resting 5 mm Hg to 16 to 21 mm Hg,79 and actively using the mouse to point and click increased the tunnel pressure to 28 to 33 mm Hg, a pressure high enough to reduce nerve blood flow.

In subjects with carpal tunnel syndrome, pressure in the carpal tunnel was 32 mm Hg with the wrist in a neutral position and rose to a mean of 110 mm Hg with full wrist extension in subjects with carpal tunnel syndrome.76 These tunnel pressures exceed the threshold of 20 to 30 mm Hg for vascular perfusion even at rest. Taken together, these findings suggest that even functional positions, such as the use of a computer keyboard and mouse, place the wrist in a position of increased carpal tunnel pressure, compromising nerve blood flow and placing people at risk for median nerve injury.

Direct damage to myelin and axons has been shown to occur with extraneural compression of as low as 50 mm Hg maintained for 2 minutes,48 and the percentage of damaged fibers increases with increasing force. Ten days after the application of compressive stress at 50 mm Hg, 30% of the axons in the region under the compressive cuff showed evidence of demyelination, focal myelin thickening, remyelination, and axonal degeneration or regeneration.48

The pathological consequences of prolonged compression include subperineurial edema; inflammation; deposition of fibrin; activation of endoneurial fibroblasts, mast cells, and macrophages; demyelination; axon degeneration; and fibrosis.83 Compression of a very long duration has been modeled in animals with loose ligatures,88 Silastic* tubes,89,90and pressure balloons placed within an anatomical tunnel.91 The pathological findings are thought to result from both inflammatory and cellular phenomena and include changes in the blood-nerve barrier, thickening of the perineurium and epineurium, thinning of myelin, demyelination and degeneration of axons in the fascicle periphery, and slowed nerve conduction velocity.

In the case of chronic compression, decompression is paramount. Physical therapy intervention should focus on reduction of inflammation, improvement in blood flow, and enhancement of the capacity of the nerve for strain and excursion along its full length in an effort to reduce the physical stress on the compressed region.

Repetitive Stresses

Vibration constitutes one form of repetitive stress. We know from studies of humans who use hand-held vibrating tools that vibration stresses can cause reductions in tactile sensation, as well as other sensory disturbances96 and reduced grip force.97,98Furthermore, myelin breakdown and fibrosis have been seen in the dorsal interosseous nerve at the wrist in people with vibration-induced neuropathy.99 Long-term exposure to vibration stresses has been shown to result in the grouping of muscle fiber types in muscle biopsies, indicative of denervation and reinnervation.98

Repetitive movements, such as those that occur in work-related musculoskeletal disorders, were discussed in detail recently by Barr and Barbe.102 The stresses placed upon the tissues may be variable in terms of type, magnitude, frequency, and duration, and the combination of these factors may place nerves in normal to extreme levels of physical stress. The chronic inflammation associated with repetitive movements places nerves under constantly higher hydrostatic compressive stress, which may increase further with contraction of the surrounding muscles. Chronic inflammation elicits within the nerves a remodeling response that seeks to add mechanical stability.103 The most common outcome is the deposition of collagen in the connective tissue layers, which leads to decreased compliance of the nerves to elongation. As with chronic compression, the approach for assessment and treatment of injuries attributable to repetitive movements must address the chronic inflammatory state and connective tissue changes. Of primary importance in interventions for all stress-induced injuries are the identification and characterization of physical stresses and the modification of their components, magnitude, time, and direction, as outlined in the physical stress theory.2

Summary

This assessment should guide treatment interventions to normalize the stresses on the nerves, be they rest, soft tissue or neurodynamic mobilization, stretching, modalities, exercise, or patient education. Treatment rationale should be based on an educated understanding of the biomechanical properties of normal and pathological nerves. The concept of a continuum of low-normal-high-excessive-extreme stresses may be used as a training tool for patient education, pointing out examples of daily activities that fall under the different categories.

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Svært interessant og bra skrevet blogg innlegg.

http://thesportsphysio.wordpress.com/2014/06/16/there-is-no-skill-in-manual-therapy-2/

For example, I learnt you can’t break down scar tissue, ‘release’ a muscle or a fascial adhesion (Chaudhry 2008, Chaudhry 2007, Schleip 2003, Threlkeld 1992)

I learnt that by stretching a muscle in a certain fashion, in a certain way, for a certain amount of time doesnt effect it’s structure (Solomonow 2007, Weppler 2010, Katalinic 2011)

I learnt that you don’t need to mobilise or manipulate a joint in a specific direction, based on a specific assessment of pain and joint feel (Chiradejnant 2003, Aquino 2009, Schomacher 2009, Nyberg 2013)

I learnt that palpation of muscles, joints, trigger points are all unreliable and can lead to questionable diagnosis that often direct treatment down wrong and ineffective pathways, I have done a blog on this particular topic recently with all the supporting evidence here.

I leant that when all the methods and techniques of manual therapy are examined through the process of systematic reviews and meta analysis most of the research is poor and even the good research shows that it doesn’t do much (Menke 2014,Kumar 2014, Artus 2010, Kent 2005)

 

The Mechanisms of Manual Therapy in the Treatment of Musculoskeletal Pain: A Comprehensive Model

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Nevner det meste rundt behandling av muskel og skjelett problemer, både usikkerheter, manglende diagnostisk spesifisitet, dårlig forhold mellom forklaringsmodelle og realitet, og foreslår nevrosentriske forklaringsmodeller. Viser til at spesifikk behandling ikke har bedre effekt enn uspesifikk behandling. Og til at den mekaniske teknikken setter igang en kaskade av nevrologiske effekter som resulterer i en behandlingeffekt.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2775050/

Abstract

Prior studies suggest manual therapy (MT) as effective in the treatment of musculoskeletal pain; however, the mechanisms through which MT exerts its effects are not established. In this paper we present a comprehensive model to direct future studies in MT. This model provides visualization of potential individual mechanisms of MT that the current literature suggests as pertinent and provides a framework for the consideration of the potential interaction between these individual mechanisms. Specifically, this model suggests that a mechanical force from MT initiates a cascade of neurophysiological responses from the peripheral and central nervous system which are then responsible for the clinical outcomes. This model provides clear direction so that future studies may provide appropriate methodology to account for multiple potential pertinent mechanisms.

Mechanical Stimulus 

First, only transient biomechanical effects are supported by studies which quantify motion (Colloca et al., 2006;Gal et al., 1997;Coppieters & Butler, 2007;Coppieters & Alshami, 2007) but not a lasting positional change (Tullberg et al., 1998;Hsieh et al., 2002). Second, biomechanical assessment is not reliable. Palpation for position and movement faults has demonstrated poor reliability (Seffinger et al., 2004;Troyanovich et al., 1998) suggesting an inability to accurately determine a specific area requiring MT.  Third, MT techniques lack precision as nerve biased techniques are not specific to a single nerve (Kleinrensink et al., 2000) and joint biased technique forces are dissipated over a large area (Herzog et al., 2001;Ross et al., 2004).

Finally, studies have reported improvements in signs and symptoms away from the site of application such as treating cervical pain with MT directed to the thoracic spine (Cleland et al., 2005;Cleland et al., 2007) and lateral epicondylitis with MT directed to the cervical spine (Vicenzino et al., 1996).

Subsequently, we suggest, that as illustrated by the model, a mechanical force is necessary to initiate a chain of neurophysiological responses which produce the outcomes associated with MT. 

Neurophysiological Mechanism 

Studies have measured associated responses of hypoalgesia and sympathetic activity following MT to suggest a mechanism of action mediated by the periaquaductal gray (Wright, 1995) and lessening of temporal summation following MT to suggest a mechanism mediated by the dorsal horn of the spinal cord (George et al., 2006) The model makes use of directly measurable associated responses to imply specific neurophysiological mechanisms when direct observations are not possible. The model categorizes neurophysiological mechanisms as those likely originating from a peripheral mechanism, spinal cord mechanisms, and/or supraspinal mechanisms.

Peripheral mechanism 

Musculoskeletal injuries induce an inflammatory response in the periphery which initiates the healing process and influences pain processing. Inflammatory mediators and peripheral nociceptors interact in response to injury and MT may directly affect this process. For example, (Teodorczyk-Injeyan et al., 2006) observed a significant reduction of blood and serum level cytokines in individuals receiving joint biased MT which was not observed in those receiving sham MT or in a control group. Additionally, changes of blood levels of β-endorphin, anandamide, N-palmitoylethanolamide, serotonin, (Degenhardt et al., 2007) and endogenous cannabinoids (McPartland et al., 2005) have been observed following MT. Finally, soft tissue biased MT has been shown to alter acute inflammation in response to exercise (Smith et al., 1994) and substance P levels in individuals with fibromyalgia (Field et al., 2002). Collectively, these studies suggest a potential mechanism of action of MT on musculoskeletal pain mediated by the peripheral nervous system for which mechanistic studies may wish to account. 

Spinal mechanisms 

MT may exert an effect on the spinal cord. For example, MT has been suggested to act as a counter irritant to modulate pain (Boal & Gillette, 2004) and joint biased MT is speculated to “bombard the central nervous system with sensory input from the muscle proprioceptors (Pickar & Wheeler, 2001).”Subsequently, a spinal cord mediated mechanism of MT must be considered and is accounted for in the model. Direct evidence for such an effect comes from a study (Malisza et al., 2003b) in which joint biased MT was applied to the lower extremity of rats following capsaicin injection. A spinal cord response was quantified by functional MRI during light touch to the hind paw. A trend was noted towards decreased activation of the dorsal horn of the spinal cord following the MT. The model uses associated neuromuscular responses following MT to provide indirect evidence for a spinal cord mediated mechanism. For example, MT is associated with hypoalgesia (George et al., 2006;Mohammadian et al., 2004;Vicenzino et al., 2001), afferent discharge (Colloca et al., 2000;Colloca et al., 2003), motoneuron pool activity (Bulbulian et al., 2002;Dishman & Burke, 2003), and changes in muscle activity (Herzog et al., 1999;Symons et al., 2000) all of which may indirectly implicate a spinal cord mediated effect.

Supraspinal mechanisms 

Finally, the pain literature suggests the influence of specific supraspinal structures in response to pain. Structures such as the anterior cingular cortex (ACC), amygdala, periaqueductal gray (PAG), and rostral ventromedial medulla (RVM) are considered instrumental in the pain experience.(Peyron et al., 2000;Vogt et al., 1996;Derbyshire et al., 1997;Iadarola et al., 1998;Hsieh et al., 1995;Oshiro et al., 2007;Moulton et al., 2005;Staud et al., 2007;Bee & Dickenson, 2007;Guo et al., 2006). Subsequently, the model considers potential supraspinal mechanisms of MT. Direct support for a supraspinal mechanism of action of MT comes from (Malisza et al., 2003a) who applied joint biased MT to the lower extremity of rats following capsaicin injection. Functional MRI of the supraspinal region quantified the response of the hind paw to light touch following the injection. A trend was noted towards decreased activation of the supraspinal regions responsible for central pain processing. The model accounts for direct measures of supraspinal activity along with associated responses such as autonomic responses (Moulson & Watson, 2006;Sterling et al., 2001;Vicenzino et al., 1998) (Delaney et al., 2002;Zhang et al., 2006), and opiod responses (Vernon et al., 1986) (Kaada & Torsteinbo, 1989) to indirectly imply a supraspinal mechanism. Additionally, variables such as placebo, expectation, and psychosocial factors may be pertinent in the mechanisms of MT (Ernst, 2000;Kaptchuk, 2002). For example expectation for the effectiveness of MT is associated with functional outcomes (Kalauokalani et al., 2001) and a recent systematic review of the literature has noted that joint biased MT is associated with improved psychological outcomes (Williams et al., 2007). For this paper we categorize such factors as neurophysiological effects related to supraspinal descending inhibition due to associated changes in the opioid system (Sauro & Greenberg, 2005), dopamine production (Fuente-Fernandez et al., 2006), and central nervous system (Petrovic et al., 2002;Wager et al., 2004;Matre et al., 2006) which have been observed in studies unrelated to MT.

Figure 3 Pathway considering both a spinal cord and supraspinal mediated effect from Bialosky et al (2008)

Moderate hypercapnia exerts beneficial effects on splanchnic energy metabolism during endotoxemia.

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Mer om den beskyttende effekten av hypercapni (økt CO2). Denne nevner at 60mmHg CO2 under bekteriell tarminfeksjon gjør at tarmene får mindre melkesyre og mindre ødeleggelse av vev.

http://www.ncbi.nlm.nih.gov/pubmed/19373455

Abstract

PURPOSE:

Low tidal volume ventilation and permissive hypercapnia are required in patients with sepsis complicated by ARDS. The effects of hypercapnia on tissue oxidative metabolism in this setting are unknown. We therefore determined the effects ofmoderate hypercapnia on markers of systemic and splanchnic oxidative metabolism in an animal model of endotoxemia.

METHODS:

Anesthetized rats maintained at a PaCO(2) of 30, 40 or 60 mmHg were challenged with endotoxin. A control group (PaCO(2) 40 mmHg) received isotonic saline. Hemodynamic variables, arterial lactate, pyruvate, and ketone bodies were measured at baseline and after 4 h. Tissue adenosine triphosphate (ATP) and lactate were measured in the small intestine and the liver after 4 h.

RESULTS:

Endotoxin resulted in low cardiac output, increased lactate/pyruvate ratio and decreased ketone body ratio. These changes were not influenced by hypercapnia, but were more severe with hypocapnia. In the liver, ATP decreased and lactate increased independently from PaCO(2) after endotoxin. In contrast, the drop of ATP and the rise in lactate triggered by endotoxin in the intestine were prevented by hypercapnia.

CONCLUSIONS:

During endotoxemia in rats, moderate hypercapnia prevents the deterioration of tissue energetics in the intestine.

Ten Steps to Understanding Manual and Movement Therapies for Pain

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Alt om smerte, kort fortalt, fra: http://www.somasimple.com/forums/showthread.php?t=4942
Nothing Simple – Ten Steps to Understanding Manual and Movement Therapies for Pain

1. Pain is a category of complex experiences, not a single sensation produced by a single stimulus.

2. Nociception (warning signals from body tissues) is neither necessary nor sufficient to produce pain. In other words, pain can occur in the absence of tissue damage.

3. A pain experience may be induced or amplified by both actual and potential threats.

4. A pain experience may involve a composite of sensory, motor, autonomic, endocrine, immune, cognitive, affective and behavioural components. Context and meaning are paramount in determining the eventual output response.

5. The brain maps peripheral and central neural processing into each of these components at multiple levels. Therapeutic input at a single level may be sufficient to resolve a threat response.

6. Manual and movement therapies may affect peripheral and central neural processes at various stages:
– transduction of nociception at peripheral sensory receptors
– transmission of nociception in the peripheral nervous system
– transmission of nociception in the central nervous system
– processing and modulation in the brain

7. Therapies that are most likely to be successful are those that address unhelpful cognitions and fear concerning the meaning of pain, introduce movement in a non-threatening internal and external context, and/or convince the brain that the threat has been resolved.

8. The corrective physiological mechanisms responsible for resolution are inherent. A therapist need only provide an appropriate environment for their expression.

9. Tissue length, form or symmetry are poor predictors of pain. The forces applied during common manual treatments for pain generally lack the necessary magnitude and specificity to achieve enduring changes in tissue length, form or symmetry. Where such mechanical effects are possible, the clinical relevance to pain is yet to be established. The predominant effects of manual therapy may be more plausibly regarded as the result of reflexive neurophysiological responses.

10. Conditioning for the purposes of fitness and function or to promote general circulation or exercise-induced analgesia can be performed concurrently but points 6 and 9 above should remain salient.

Bibliography

Books:
Pain: The Science of Suffering – Patrick Wall
The Challenge of Pain – Patrick Wall, Ronald Melzack
Explain Pain – David Butler, Lorimer Moseley
The Sensitive Nervous System – David Butler
Phantoms in the Brain – V. S. Ramachandran
Topical Issues in Pain Vol’s 1-5 – Louis Giffiord (ed)
The Feeling of What Happens – Antonio Damasio
Clinical Neurodynamics – Michael Shacklock
Eyal Lederman – The Science and Practice of Manual Therapy

Research articles:
Melzack R. Pain and the neuromatrix in the brain. J Dental Ed. 2001;65:1378-82.
Craig AD. Pain mechanisms: Labeled lines versus convergence in central processing. Ann Rev Neurosci. 2003;26:130.
Craig AD. How do you feel? Interoception: the sense of the physiological condition of the body. Nature Rev Neurosci. 2002;3:655-66.
Henderson LA, Gandevia SC, Macefield VG. Somatotopic organization of the processing of muscle and cutaneous pain in the left and right insula cortex: A single-trial fMRI study. Pain. 2007;128:20-30.
Olausson H, Lamarre Y, Backlund H, Morin C, Wallin BG, Starck G, Ekholm S, Strigo I, Worsley K, Vallbo AB, Bushnell MC. Unmyelinated tactile afferents signal touch and project to insular cortex. Nature Neurosci. 2002;5:900–904.
Moseley GL. A pain neuromatrix approach to patients with chronic pain. Manual Ther. 2003;8:130-40.
Moseley GL. Unravelling the barriers to reconceptualisation of the problem in chronic pain: The actual and perceived ability of patients and health professionals to understand the neurophysiology. J Pain. 2003;4:184-89.
Moseley GL, Arntz A. The context of a noxious stimulus affects the pain it evokes. Pain. 2007;133(1-3):64-71.
Moseley, GL, Nicholas, MK and Hodges, PW. A randomized controlled trial of intensive neurophysiology education in chronic low back pain. Clin J Pain. 2004;20:324-30.
Crombez G, Vlaeyen JWS, Heuts PH et al. Pain-related fear is more disabling than pain itself. Evidence on the role of pain-related fear in chronic back pain disability. Pain. 1999;80:329-40.
Zusman M. Forebrain-mediated sensitization of central pain pathways: ‘non-specific’ pain and a new image for manual therapy. Manual Ther. 2002;7:80-88.
Dorko B. The analgesia of movement: Ideomotor activity and manual care. J Osteopathic Med. 2003;6:93-95.
Threlkeld AJ. The effects of manual therapy on connective tissue. Phys Ther. 1992;72:893-902.
Lederman E. The myth of core stability. Retrieved at: http://www.ppaonline.co.uk/

THE VALUE OF BLOWING UP A BALLOON

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Dette er en veldig viktig artikkel for å forstå diafragmas rolle i både pust og bevegelse, og ifh smertetilstander i ryggraden. Nevner en lovende teknikk for å styrke diafragma og støttemuskulatur hvor man blåser opp en ballong og strammer kjernemuskulaturen. Nevner Zone of Apposition (ZOA) som beskriver diafragmas bevegelsesmuligheter. Ved lav ZOA har diafrgma lite bevegelse. Vi ønsker å øke ZOA. Denne øvelsen er konstruert basert på fysioterapeutisk prinsipper, men i Verkstedet Breathing System har vi øvelser som er gir samme resultater på diafragma, men bygget på lang og erfaringsbasert tradisjon fra tibetansk buddhisme.

Nevner også hvordan mage-pust minker bevegelsen i diafragma.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2971640/

Suboptimal breathing patterns and impairments of posture and trunk stability are often associated with musculoskeletal complaints such as low back pain. A therapeutic exercise that promotes optimal posture (diaphragm and lumbar spine position), and neuromuscular control of the deep abdominals, diaphragm, and pelvic floor (lumbar-pelvic stabilization) is desirable for utilization with patients who demonstrate suboptimal respiration and posture. This clinical suggestion presents a therapeutic exercise called the 90/90 bridge with ball and balloon. This exercise was designed to optimize breathing and enhance both posture and stability in order to improve function and/or decrease pain. Research and theory related to the technique are also discussed.

Many muscles used for postural control/stabilization and for respiration are the same, for example: the diaphragm, transversus abdominis, and muscles comprising the pelvic floor.1–6 Maintaining optimal posture/stability and respiration is important and is even more challenging during exercise. Exercise increases respiratory demand (e.g. running) and limb movements (e.g. arms moving while standing still) increase postural demands for stabilization.3,7

Many factors are potentially involved with suboptimal respiration and suboptimal (faulty) posture and may be associated with musculoskeletal complaints such as low back pain, and/or sacroiliac joint pain.8 (Table 1)

Suboptimal Respiration and Posture
Decreased/suboptimal Zone of Apposition of diaphragm
Decreased exercise tolerance
Decreased intra-abdominal pressure
Shortness of Breath/Dyspnea
Decreased respiratory efficiency
Decreased expansion of lower rib cage/chest
Decreased appositional diaphragm force
Decreased length of diaphragm (short)
Decreased transdiaphragm pressure
Increased use of accessory muscles of respiration
Poor neuromuscular control of core muscles
Increased lumbar lordosis
Increased anterior pelvic tilt
Increased hamstring length
Increased abdominal length
Rib elevation/external rotation
Sternum elevation
Increased activity of paraspinals
Increased lumbar-pelvic instability
Low back pain
Sacroiliac Joint pain
Thoracic Outlet Syndrome
Headaches
Asthma

One of the most critical factors, often overlooked by physical therapists, is maintaining an optimal zone of apposition of the diaphragm.3,9–11 The zone of apposition (ZOA) is the area of the diaphragm encompassing the cylindrical portion (the part of the muscle shaped like a dome/umbrella) which corresponds to the portion directly apposed to the inner aspect of the lower rib cage.12 The ZOA is important because it is controlled by the abdominal muscles and directs diaphragmatic tension. When the ZOA is decreased or suboptimal, there are several potential negative consequences. (Table 1) Two examples include:

  1. Inefficient respiration (less air in and out) because the transdiaphragmatic pressure is reduced.11 The smaller the ZOA, there will be less inspiratory action of the diaphragm on the rib cage.11
  2. Diminished activation of the transversus abdominis which is important for both respiration and lumbar stabilization.11,13

The incidence of LBP has been documented to be as high as 30% in the athletic population, and in many cases pain may persist for years.15 Low back pain is frequently correlated with faulty posture such as an excessive lumbar lordosis.16–18 Excessive lumbar lordosis may be associated with over lengthened and weak abdominal musculature.18–20 Poor neuromuscular control of core muscles (transversus abdominis, internal oblique, pelvic floor and diaphragm) has been described in individuals with SIJ pain21 and in individuals with lumbar segmental instability, potentially adversely affecting respiration.22

Richardson et al.27 describe coordination of the Transversus abdominis and the diaphragm in respiration during tasks in which stability is maintained by tonic activity of these muscles. During inspiration, the diaphragm contracts concentrically, whereas the transversus abdominis contracts eccentrically. The muscles function in reverse during exhalation with the diaphragm contracting eccentrically while the transversus abdominis contracts concentrically. Hodges et al. noted that during respiratory disease the coordinating function between the transversus abdominis and diaphragm was reduced.6 Thus, it is also possible that faulty posture such as over lengthened abdominals and excessive lordosis could reduce the coordination of the diaphragm and transversus abdominis during respiration and stabilization activities.

O’sullivan et al.21 studied subjects with LBP attributed to the sacroiliac joints and compared them to control subjects without pain. O’sullivan et al. compared respiratory rate and diaphragm and pelvic floor movement using real time ultrasound during a task that required load transfer through the lumbo-pelvic region (the active straight leg raise test). Subjects with pain had an increase in respiratory rate, descent of their pelvic floor and a decrease in diaphragm excursion as compared to the control subjects, who had normal respiratory rates, less pelvic floor descent, and optimal diaphragm excursion. While O’sullivan et al. concluded that an intervention program focused on integrating control of deep abdominal muscles with normal pelvic floor and diaphragm function may be effective in managing patients with LBP,21 they did not describe strategies or exercises to achieve this goal.21

While the role of the Transversus abdominis in lumbar stability is well documented, less well known is the role of the diaphragm in lumbar stability. While the primary function of the diaphragm is respiration, it also plays a role in spinal stability.3,28

The right hemidiaphragm attaches distally to the anterior portions of the first through third lumbar vertebrae (L1-3) and the left hemidiaphragm attaches distally on the first and second lumbar vertebrae (L1-2).29 This section of the diaphragm is referred to as the crura. Of interest is the asymmetrical attachment of the diaphragm with the left hemidiaphragm attaching to L1-2 and the right portion attaching to L1-3.

During the inhalation phase of ventilation, the dome of the diaphragm moves caudally like a piston creating a negative pressure in the thorax that forces air into the lungs. This action is normally accompanied by a rotation of the ribs outward (external rotation) largely in part due to the ZOA.12 (Figure 1) Apposition is a term that means multiple layers adjacent to each other.33 The normal force of pull on the sternal and costal portions of the diaphragm would produce an internal rotation of the ribs. The ZOA creates an external rotation of these ribs primarily because the pressure in the thoracic cavity prevents an inward motion. The crural portion of the diaphragm assists the caudal motion of the dome. It also pulls the anterior lumbar spine upward (cephalad and anterior). Additionally, the abdominal muscles and pelvic floor musculature are less active to allow visceral displacement due to the dome of the diaphragm dropping. With exhalation, this process is reversed. Abdominal muscle activity compresses the viscera in the abdominal cavity, the diaphragm is forced cephalad and the ribs internally rotate. As exhalation becomes forced as during exercise, abdominal activity (rectus abdominus, internal obliques, external obliques, and transversus abdominis) will be increased.34–36

When the ZOA is optimized, the respiratory and postural roles of the diaphragm have maximal efficiency.37 In suboptimal positions (i.e. decreased ZOA), the diaphragm has a decreased ability to draw air into the thorax because of less caudal movement upon contraction and less effective tangential tension of the diaphragm on the ribs and therefore lower transdiaphragmatic pressure.38 This decreased ZOA is accompanied by decreased expansion of the rib cage, postural alterations, and a compensatory increase in abdominal expansion.12 (Figure 2)

One such adaptive breathing strategy would be to relax the abdominal musculature more than necessary on inspiration to allow for thoraco-abdominal expansion. This situation leads to decreased abdominal responsibility while breathing and can contribute to instability. This would reflect more upper chest breathing and less efficient diaphragm activity. If the body maintains this position and breathing strategy for an extended period of time, the diaphragm may adaptively shorten and the lungs may become hyperinflated.37,39,40 Hyperinflation may also contribute to over use of accessory muscles of respiration such as scalenes, sternocleidomastoid (SCM), pectorals, upper trapezius and paraspinals in an attempt to expand the upper rib cage.41–44 Again, without an optimal dome shape/position of the diaphragm or an optimal ZOA the body compensates to get air in with accessory muscles since the more linear/flat/short diaphragm is less efficient for breathing.32

Instructions for Performance of the 90/90 Bridge with Ball and Balloon: 1. Lie on your back with your feet flat on a wall and knees and hips bent at a 90-degree angle. 2. Place a 4-6 inch ball between your knees. 3. Place your right arm above your head and a balloon in your left hand. 4. Inhale through your nose and as you exhale through your mouth, perform a pelvic tilt so that your tailbone is raised slightly off the mat. Keep low back flat on the mat. Do not press your feet into the wall, instead pull down with your heels. 5. You should feel the back of your thighs and inner thighs engage, keeping pressure on the ball. Maintain this position for the remainder of the exercise. 6. Now inhale through your nose and slowly blow out into the balloon. 7. Pause three seconds with your tongue positioned on the roof of your mouth to prevent airflow out of the balloon. 8. Without pinching the neck of the balloon and keeping your tongue on the roof of your mouth, inhale again through your nose. 9. Slowly blow out as you stabilize the balloon with your left hand. 10. Do not strain your neck or cheeks as you blow. 11. After the fourth breath in, pinch the balloon neck and remove it from your mouth. Let the air out of the balloon.12. Relax and repeat the sequence 4 more times. Copyright © Postural Restoration Institute™ 2009, used with permission

The patient/athlete is asked to hold the balloon with one hand and inhale through his/her nose with the tongue on the roof of the mouth (normal rest position) and then exhale through his/her mouth into the balloon. The inhalation, to about 75% of maximum, is typically 3-4 seconds in duration, and the complete exhalation is usually 5-8 seconds long followed by a 2-3 second pause. This slowed breathing is thought to further relax the neuromuscular system/parasympathetic nervous system and generally decrease resting muscle tone. Ideally the patient/athlete will be able to inhale again without pinching off the balloon with their teeth, lips, or fingertips. This requires maintenance of intra-abdominal pressure to allow inhalation through the nose without the air coming back out of the balloon and into the mouth.

When the exercise is performed by the patient/athlete with hamstring and gluteus maximus (glut max) activation (hip extensors) the pelvis moves into a relative posterior pelvic tilt and the ribs into relative depression and internal rotation. This pelvic and rib position helps to optimize abdominal length (decreases) and diaphragm length/ZOA (increases).

Clinical experience with the BBE includes utilization of the exercise for both female and male patients (more females than males), ages 5-89 with a wide variety of diagnoses including: low back pain, trochanteric bursitis, SIJ pain, asthma, COPD, acetabular labral tear, anterior knee pain, thoracic outlet syndrome (TOS) and sciatica.

Understanding the Process of Fascial Unwinding

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Studie som nevner hvordan «fascial unwinding» skjer ved hjelp av stimulering av mekanoreseptorer i huden. Parasympatikus aktiveres og gjør at muskelspenninger slipper taket.

http://ijtmb.org/index.php/ijtmb/article/view/43/75

Hypothetical Model: During fascial unwinding, the therapist stimulates mechanoreceptors in the fascia by applying gentle touch and stretching. Touch and stretching induce relaxation and activate the parasympathetic nervous system. They also activate the central nervous system, which is involved in the modulation of muscle tone as well as movement. As a result, the central nervous system is aroused and thereby responds by encouraging muscles to find an easier, or more relaxed, position and by introducing the ideomotor action. Although the ideomotor action is generated via normal voluntary motor control systems, it is altered and experienced as an involuntary response.

Conclusions: Fascial unwinding occurs when a physically induced suggestion by a therapist prompts ideomotor action that the client experiences as involuntary. This action is guided by the central nervous system, which produces continuous action until a state of ease is reached. Consequently, fascial unwinding can be thought of as a neurobiologic process employing the self-regulation dynamic system theory.

In this paper, I propose a model based on scientific literature to explain the process and mechanism of fascial unwinding (Fig. 1). The model is based on the theories of ideomotor action by Carpenter(18) and Dorko,(16) fascia neurobiologic theory by Schleip,(4,5) and the psychology of consciousness by Halligan and Oakley.(19)

A set of conditions are required to initiate or facilitate the unwinding process. The therapist’s sensitivity and fine palpation skills form the most important part of these conditions, but it is also imperative that the client be able to relax and “let go” of his or her body.

In the first stage—the initiation or induction phase— the therapist working on a client will introduce touch or stretching onto the tissue. Touch is the entrance requirement for the process of unwinding. Touch stimulates the fascia’s mechanoreceptors and, in turn, arouses a parasympathetic nervous system response.(5) As a result of this latter response, the client is in a state of deep relaxation and calm, sometimes followed with rapid eye movement, twitching, or deep breathing—a state that can be observed clinically.(20,21) In this state, the conscious mind is relaxed and off guard. Stimulation of mechanoreceptors also influences the central nervous system. The central nervous system responds to this proprioceptive input by allowing the muscles to perform actions that decrease tone or that create movement in a joint or limb, making it move into an area of ease. At this point, ideomotor reflexes occur. Ideomotor action pertains to involuntary muscle movement, which can manifest in various ways and is directed at the central nervous system.(22)

These reflexes occur unconsciously, indicating dissociation between voluntary action and conscious experience.(23) In clinical situations, the client is unaware of the unconscious movement and thinks that it is generated by the therapist. This unconscious movement or stretching sensation stimulates a response in the tissue, providing a feedback to the central nervous system as outlined in the theory of ideomotor action.(24) The process is repeated until the client is relaxed or has reached a “still point” or state of ease.

The indirect stimulation of the autonomic nervous system (that is, the parasympathetic nervous system), which results in global muscle relaxation and a more peaceful state of mind, represents the heart of the changes that are so vital to many manual therapies. Gentler types of myofascial stretching and cranial techniques have also long been acknowledged to affect the parasympathetic nervous system.(25) Bertolucci(20) observed that, when a client is being treated with a muscle repositioning technique, the client begins to show involuntary motor reactions—reactions that include the involuntary action of related muscles and rapid eye movements. Several studies have evaluated the physiologic changes in the autonomic nervous system that occur as a result of craniosacral and MFR interventions,(21,26) clinically-known techniques that can trigger the unwinding process.

Recent studies have used heart rate variability, respiratory rate, skin conductance, and skin temperature as measures of physiologic change. Zullow and Reisman(26) indicated an increase in parasympathetic activity resulting from the compression of the fourth intracranial ventricle (CV4) maneuver and sacral holds, as measured by heart rate variability. Using heart rate variability measurement, Henley et al.(25) demonstrated that cervical MFR shifts sympathovagal balance from the sympathetic to the parasympathetic nervous system.

Dorko(16) was the first to suggest that fascial unwinding can be simply explained as an ideomotor movement. McCarthy et al.(29) were the first to document unwinding as an ideomotor-based manual therapy in the treatment of a patient with chronic neck pain. Their research showed that a reduction in pain intensity and perceived disability can be achieved with the introduction of ideomotor treatment.

A model built upon the neurobiologic, ideomotor action, and consciousness theories is proposed to explain the mechanism of unwinding. Touch, stretching, and manual therapy can induce relaxation in the parasympathetic nervous system. They also activate the central nervous system, which is involved in the modulation of muscle tone as well as movement. This activation stimulates the response to stretching: muscles find areas and positions of ease, the client experiences less pain or is more relaxed, thereby introducing the ideomotor action. The ideomotor action is generated through normal voluntary motor control systems, but is altered and experienced as an involuntary reaction. The stretching sensation provides a feedback to the nervous system, which in turn will generate the movements again.

Three-Dimensional Mathematical Model for Deformation of Human Fasciae in Manual Therapy

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Spennende studie som viser at tykkere bindevevsområder som fascia latae og plantar fascia ikke kan deformeres i strukturell integrering, men mykere bindevev som f.eks. rundt nesen kan det. Den forteller at det kreves enormt med strykk og strekk for å skape endringer i bindevev, så den releasen for opplever i strukturell integrering er sannsynligvis heller endringer i «twisting or extension forces» i vevet. Bindevevet blir ikke lengre eller deformert på noen som helst måte, det blir mer fleksibelt.
http://www.jaoa.org/content/108/8/379.long

The palpable sensations of tissue release that are often reported by osteopathic physicians and other manual therapists cannot be due to deformations produced in the firm tissues of plantar fascia and fascia lata. However, palpable tissue release could result from deformation in softer tissues, such as superficial nasal fascia.

Previous SectionNext Section

 

Rolfing, which is also referred to as structural integration in osteopathic medicine, is a manual technique in which the practitioner is trained to observe both obvious movement of the skeleton and more subtle motion evidenced by slight muscle contraction visible through the overlying skin.1,22 Rolfers are not trained in diagnosis and treatment of specific conditions—as are osteopathic physicians—but rather in therapies to improve posture and general ease of function.1,22

The therapist manipulated the nasal fascia of the subject with two fingers oriented caudally at a 30-degree angle to the surface of the skin just superior to the cartilaginous structure of the nose. Both normal and tangential pressure were applied with the rolfing technique (ie, structural integration).1

We used available in vitro data for dense fasciae7,11 to evaluate the magnitude of forces required to produce specific deformations in these fasciae. We concluded that the magnitude of these evaluated forces is outside the physiologic range of manual therapy. This conclusion is supported by the findings of Sucher et al6 that in vitro manipulation of the carpal tunnel area on human cadavers leads to plastic deformation only if the manipulation is extremely forceful or lasts for several hours.

Ward25 describes manual techniques central to osteopathic medicine (integrated neuromusculoskeletal release, myofascial release) that are designed to stretch and reflexively release restrictions in soft tissue. These techniques incorporate fascial compression, shear, traction, and twist. Our results indicate that compression and shear alone, within the normal physiologic range, cannot directly deform the dense tissue of fascia lata and plantar fascia, but these forces can impact softer tissue, such as superficial nasal fascia.

Our calculations reveal that the dense tissues of plantar fascia and fascia lata require very large forces—far outside the human physiologic range—to produce even 1% compression and 1% shear. However, softer tissues, such as superficial nasal fascia, deform under strong forces that may be at the upper bounds of physiologic limits. Although some manual therapists3,4 anecdotally report palpable tissue release in dense fasciae, such observations are probably not caused by deformations produced by compression or shear. Rather, these palpable effects are more likely the result of reflexive changes in the tissue—or changes in twisting or extension forces in the tissue.25