Stikkordarkiv: Behandling

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The trigger point strikes … out!

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En blog av Quinter som bedre forklarer det nevrologiske utgangspunktet for triggerpunkter, eller mer korrekt: ømme punkter og stramme muskler.

Basert på deres nye forklaringsmodell vil et problem (f.eks. betennelse) lenger inn på en sensorisk nerve sender betennelse (nevrogen betennelse) ut til muskelen, i tillegg til at motoriske og sympatiske (stress) signaler fra ryggmargen sendes ut til muskelen og gir en muskelspenning og twitchrespons vi kan se og kjenne med fingrene.

Ang. nevrogen betennelse så nevner wikipedia en studie på mus som viser at magnesium mangel, selv det som er innenfor «normalen» kan bidra til økt utskillelse av SP, som er en nevrogen betennelsesfaktor. http://en.wikipedia.org/wiki/Neurogenic_inflammation

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But when I met the late Bob Elvey, he completely changed my way of thinking about these clinical problems. Bob’s mantra was that “muscles protect nerves.” He introduced me to the dynamics of the nervous system and I came to understand that peripheral nerves of the upper limb had evolved to be able to adapt to the various changes in limb position and length and that they were vulnerable at certain anatomical points along their course.

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In brief, Geoff’s studies have had two major impacts on how we think about pain felt in muscles or other deep structures.

Firstly, he confirmed the presence of nociceptors with multiple receptive fields that branch within the nerve sheaths and extend to other deep tissues (nervi nervorum) [7]. The implication of this finding is that activity in a receptor in one structure such as the nerve sheath, could be perceived in another, such as the muscle.

Secondly, he showed that inflammation of nerves has profound effects on these same axons, the nociceptors to deep structures. These effects include ongoing activity and abnormal mechanical sensitivity [8, and others]. The implication of this finding is that this activity will be perceived by the brain in the area of the receptive fields mapped for the deep structure nociceptors, not in the area of the problem.

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Figure 1. Proposed hypothesis for the development of focal muscle sensitivity and possible alteration in muscle texture with a proximal neural cause. Inflammation affecting a peripheral nerve (red spot) results in spontaneous and mechanically evoked afferent and efferent action potentials in small caliber sensory neurons innervating non-cutaneous structures, and decreased sympathetic discharge (-). These processes may cause reflex motor discharge sufficient to cause a palpable contraction (?), which combined with clinical phenomena associated with neurogenic inflammation (+), could explain the clinical phenomenon that has become known as a “trigger point.”

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Guideline for diagnosis and treatment of subacromial pain syndrome

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Beskriver det meste om behandling av innklemninger som fører til smerter når man løfter armen. Alle studier på behandling har blitt gradert med «level of evidence», hvor 1 er best. Operative inngrep har fått evensgrad 3, altså svært dårlig, selv når det er snakk om Rotator Cuff Tear.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4062801/

1. A diagnosis of SAPS can only be made after a combination of tests; the Hawkins-Kennedy test, the painful arc test, and the infraspinatus muscle strength test are advisable.

5. Prescribe therapy or home exercises of low intensity and high frequency, combining eccentric training with stabilization training of the scapula and focusing on relaxation and proper posture.

6. Treatment of myofascial trigger points (including stretching of the muscles) can support exercise therapy.

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Vibration and pressure wave therapy for calf strains: a proposed treatment

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Denne nevner også veldig mye interessant om Segmental Vibration Therapy, og benytter seg av en maskin som ligner Percussor. Nevner bl.a. at betennelses faktorer, som IL-6 og CRP, går ned

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711703/

Summary

Calf (lower leg) strains have a variety of treatment regimens with variable outcomes and return to activity (RTA) time frames. These injuries involve disruption of portions or the entire gastrocnemius-soleus myo-tendinous complex. Conservative treatment initially consists of rest, ice, compression, elevation (RICE). Immediately following calf injury, patients can utilize cryotherapy, massage, passive range of motion, and progressive exercise. In general, Grade I through Grade III calf strains can take up to 6 weeks before the athlete can return to training. It can also involve the loss of more than 50% of muscle integrity. Recently, vibration therapy and radial pressure waves have been utilized to treat muscular strains and other myo-tendinous injuries that involve trigger points. Studies have suggested vibration therapy with rehabilitation can increase muscle strength and flexibility in patients. Segmental vibration therapy (SVT) is treatment to a more focal area. Vibration therapy (VT) is applied directly to the area of injury. VT is a mechanical stimulus that is thought to stimulate the sensory receptors, as well as decrease inflammatory cells and receptors. Therefore, VT could be a valuable tool in treating athlete effectively and decreasing their recovery time. The purpose of this paper is to give the reader baseline knowledge of VT and propose a treatment protocol for calf strains using this technology along with radial pressure waves.

Findings also showed a decrease in IL6 at five days after an increase at the first 24 hours as compared to the control group. There was a decrease in CRP and Histamine at five days. Broadbent et al. related the CPK findings were unclear4.

treatment showed increase ROM at the ankle, and increased hamstring flexibility compared to the post control treatment as well as baseline. There was also a decrease in stiffness at the ankle as well as the hamstring after SVT.

 

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Immediate effects of breathing re-education on respiratory function and range of motion in chronic neck pain.

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Å lære seg å bruke riktige pustemuskler gir mindre muskelspenninger og bedre bevegelighet i nakken. Om diafragma, den viktigste pustemuskelen, er svak eller på en eller annen måte ikke blir brukt nok, vil nakkemusker ta over store deler av pustefunksjonen. Dette kan være grunnlag til mange plager i nakken.

I denne studien gjorde 36 mennesker 30 minutter pustetrening. Smertenivåer og muskelspenninger ble redusert, og bevegelse i brystkassen og i nakken ble økt. 

Med enkle øvelser kan man få store resultater. Kun 30 minutter er nok! Om man gjør øvelser hver dag og diafragma blir sterke så trengs det mye mindre tid også.

http://www.ncbi.nlm.nih.gov/pubmed/25141528/

CONCLUSION:

Breathing re-education can change breathing patterns and increase chest expansion. This change leads to an improvement in CROM Positive consequences may result from the improvement in diaphragm contraction or reduced activity of accessory muscles.

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The meaning of mechanically produced responses

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Fra 1994, forskeren Max Zusman. Nevner veldig mange interessante perspektiver på hvordan mekanisk stimuli (percussor, DNM, SI, osv) demper smerte.

http://www.sciencedirect.com/science/article/pii/S0004951414604529

Abstract: The precise source and cause of mechanically evoked sensory and motor responses can sometimes be surprisingly difficult to identify. Accurate interpretation of these responses may be confounded by peripheral as well as central nervous system mechanisms. Examples of such peripheral nervous system mechanisms likely to be of relevance to therapists have been selected from basic and clinical research. Symptomatic relief has been inferred to endorse the diagnostic specificity of mechanical stimulation. The extent to which this would be valid for relief acquired by neurological means is discussed in terms of endogenous pain inhibitory systems

Some degree of local inhibition with mechanical stimuli delivered directly to a pathological site may be mainly a consequence of supplementary input in large diameter cutaneous afferents. Unlike those afferents supplying deep tissue such as joint, muscle etc., small diameter cutaneous afferents appear to be largely impervious to mechanical sensitisation by chemical mediators of the inflammatory response (Handwerker and Reeh 1991).

Therefore, mechanical stimulus parameters which maximise large diameter afferent input from the skin and at the same time minimise sensitised small diameter afferent input from deep tissue such as joint, muscle etc. would be therapeutically effective

Spontaneously occurring clinically relevant symptoms and signs are ultimately a product of both peripheral and central nervous system mechanisms. As  such, they are complexly derived and displayed. Their true origin and significance are sometimes obscure and liable to misinterpretation. Rather than being invariably diagnostically definitive, provocative mechanical manoeuvres can compound these uncertainties. The provocative mechanical manoeuvres used by therapists are, neurologically speaking, relatively crude. They do not have the necessary specificity to always distinguish between pathologically and non pathologically involved tissues and sites, Since their specific systemic effects have not been investigated,  the responses produced with such stimuli are subject to variously influenced and informed interpretation.

The reasons for symptomatic relief produced asa result of these mechanical manoeuvres are not known for certain. Neurologically, this appears to involve inhibitions in the central nervous system. Input conveyed centrally by different classes of primary afferents stimulated at a variety of sites has the potential to produce therapeutically effective inhibitions. Mechanical provocation can confirm the presence of clinically relevant sensory and motor responses. However, understanding what these responses might actually mean in terms of their source and cause would frequently require additional input from the basic sciences.

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Diagnosis and management of adhesive capsulitis

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Nevner det meste av medisinske behandlingsmetoder for frozen shoulder. Men kun medisiner eller kirurgi nevnes. Bedring fra 92% til 165% fremad elevasjon stående, og fra 12% til 52% utrotasjon av armen ryggliggende er resultatene av kirurgi. Dette har jeg også fått til ved hjelp av dry needling og behandlingene på Verkstedet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2682415/

Adhesive capsulitis is diagnosed by numerous physical characteristics including a thickening of the synovial capsule, adhesions within the subacromial or subdeltoid bursa, adhesions to the biceps tendon, and/or obliteration of the axillary fold secondary to adhesions [1–9].

Adhesive capsulitis has an incidence of 3–5% in the general population and up to 20% in those with diabetes. This disorder is one of the most common musculoskeletal problems seen in orthopedics [11–15]. Although some have described adhesive capsulitis as a self-limiting disorder that resolves in 1–3 years [13, 16–20], other studies report ranges of between 20 and 50% of patients with adhesive caspulitis which suffer long-term ROM deficits that may last up to 10 years [21–25].

Adhesive capsulitis is commonly associated with other systemic and nonsystemic conditions. By far the most common is the co-morbid condition of diabetes mellitus, with an incidence of 10–36% [14, 27, 28].

Other co-morbid conditions include hyperthyroidism, hypothyroidism, hypoadrenalism, Parkinson’s disease, cardiac disease, pulmonary disease, stroke, and even surgical procedures that do not affect the shoulder such as cardiac surgery, cardiac catheterization, neurosurgery, and radical neck dissection [29–39].

Adhesive capsulitis is classified into two categories: (1) primary, which is insidious and idiopathic, or (2) secondary, which is generally due to trauma or subsequent immobilization [41]. Those with primary adhesive capsulitis generally have a very gradual onset and progression of symptoms, with no known precipitating event that can be identified [42].

Adhesive capsulitis presentation is generally broken into three distinct stages [43]. The first stage that is described is called the freezing or painful stage. Patients may not present during this stage because they think that eventually the pain will resolve if self-treated.

This phase typically lasts between 3 and 9 months and is characterized by an acute synovitis of the glenohumeral joint [44].

Most patients will progress to the second stage, the frozen or transitional stage. During this stage shoulder pain does not necessarily worsen. Because of pain at end ROM, use of the arm may be limited causing muscular disuse. The frozen stage lasts anywhere 4 to 12 months [44].

The third stage begins when ROM begins to improve. This 3rd stage is termed the thawing stage. This stage lasts anywhere from 12 to 42 months and is defined by a gradual return of shoulder mobility.

Pain associated with adhesive capsulitis can cause a limitation or selective immobilization of the painful shoulder. Prolonged immobilization of a joint has been shown to cause several detrimental pathophysiologic findings including: decreased collagen length, fibrofatty infiltration into the capsular recess, ligament atrophy resulting in decreased stress absorption, collagen band bridging across recesses, random collagen production, and altered sarcomere number in muscle tissue [45].

Testing for impingement may be positive with a Hawkin’s or Neer sign; however, the pain is likely from the intrinsic process of impingement or capsular stretch rather than from adhesive capsulitis.

The diagnosis of adhesive capsulitis is often one of exclusion. Early in the disease process adhesive capsulitis may clinically appear similar to other shoulder conditions such as major trauma, rotator cuff tear, rotator cuff contusion, labral tear, bone contusion, subacromial bursitis, cervical or peripheral neuropathy. Additionally, a history of a previous surgical procedure can lead to shoulder stiffness. If a history of these other pathologies are negative and if radiographs do not demonstrate osteoarthritis, then the diagnosis can be given.

Non-operative treatment

Anti-inflammatories

Treatment of adhesive capsulitis often involves the use of anti-inflammatories, or corticosteroids. NSAIDs may be used during any phase as an attempt to relieve symptoms. There are no well done studies to indicate that NSAIDs change the natural history of adhesive capsulitis.

Intra-articular corticosteroid injections

Although high-quality randomized studies of corticosteroid injection for treatment of adhesive capsulitis have not been done, there is some evidence to indicate there is a short-term benefit with their use.

Surgical treatment

The treatment of adhesive capsulitis should lead to the operating room only after a concerted effort at conservative management has failed.

Manipulation under anesthesia

Manipulation under anesthesia as a means of treatment has been advocated. This method allows return of ROM in the operating room. Immediate postoperative physical therapy can be initiated with this form of treatment [49]. Manipulation under anesthesia has the disadvantage in that tissues that are stretched while the patient is under anesthesia may cause pain when awake. This can potentially slow recovery. When surgical release is added to this procedure it induces further surgical trauma to the shoulder and may slow rehabilitation.

Arthroscopic release and repair

Arthroscopy is an excellent additional tool for addressing the shoulder with adhesive capsulitis, and has become well accepted in treating this process. The essential lesion is the tightened coracohumeral ligament and rotator interval with the contracted capsule including the axillary pouch. These structures can be treated by release with arthroscopic instruments.

Operative treatment of adhesive capsulitis has been shown to decrease the duration of the disease and to return ROM with good success. Total recovery of pain-free ROM averages 2.8 months (1–6), and time for formal physical therapy averages 2.3 months (2–20) weeks. Forward elevation improved from the average of 92–165° and external rotation with the elbow at the side improved from 12 to 56° in a series of 68 shoulders treated with arthroscopic capsular release [61].

Patient education

Because adhesive capsulitis is so painful and has a very slow progression of resolution, patient education is critical for success. Patients should be educated in the chronicity of this condition. If they know and understand ahead of time that it can be several years before symptoms are completely resolved, apprehension and a feeling of urgency for functional return may be decreased.

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Trigger point dry needling as an adjunct treatment for a patient with adhesive capsulitis of the shoulder.

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Nevner at dry needling gir en raskere smertereduksjon og bevegelsesøkning ved frozen shoulder. 10 behandlinger ble gjort i dette tilfelle.

http://www.ncbi.nlm.nih.gov/pubmed/24261931

 

BACKGROUND:

Prognosis for adhesive capsulitis has been described as self-limiting and can persist for 1 to 3 years. Conservative treatment that includes physical therapy is commonly advised.

CASE DESCRIPTION:

The patient was a 54-year-old woman with primary symptoms of shoulder pain and loss of motion consistent with adhesive capsulitis. Manual physical therapy intervention initially consisted of joint mobilizations of the shoulder region and thrust manipulation of the cervicothoracic region. Although manual techniques seemed to result in some early functional improvement, continued progression was limited by pain. Subsequent examination identified trigger points in the upper trapezius, levator scapula, deltoid, and infraspinatus muscles, which were treated with dry needling to decrease pain and allow for higher grades of manual intervention.

OUTCOMES:

The patient was treated for a total of 13 visits over a 6-week period. After trigger point dry needling was introduced on the third visit, improvements in pain-free shoulder range of motion and functional outcome measures, assessed with the Shoulder Pain and Disability Index and the shortened form of the Disabilities of the Arm, Shoulder and Hand questionnaire, exceeded the minimal clinically important difference after 2 treatment sessions. At discharge, the patient had achieved significant improvements inshoulder range of motion in all planes, and outcome measures were significantly improved.

DISCUSSION:

This case report describes the clinical reasoning behind the use of trigger point dry needlingin the treatment of a patient with adhesive capsulitis. The rapid improvement seen in this patient following the initiation of dry needling to the upper trapezius, levator scapula, deltoid, and infraspinatus muscles suggests that surrounding muscles may be a significant source of pain in this condition.

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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)

 

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Care and Feeding of the Endocannabinoid System: A Systematic Review of Potential Clinical Interventions that Upregulate the Endocannabinoid System

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Denne beskriver endocannabinoider(eCB) og hvordan man kan øke produksjonen av dem og reseptorene for dem. eCB er et kroppens viktigste naturlige smertstillende stoffer som kan produseres og påvirker alle nerver i kroppen. Spesielt viktig i hjernen, men også i det perifere nervesystem.

Massasje, kiropraktikk og hard trening (f.eks. runners high) utløser eCB i kroppen. Det gjør også omegabalanse (mer n-3), probiotica, NSAIDs, m.m. Også yoga, meditasjon, pust og andre stressreduserende påvirker eCB. Og trening, men kun om man gjør det jevnlig over tid.

Den nevner at langvarig stress reduserer eCB i kroppen siden det er koblet til kortisol. Men den nevner også at noen tilstander kan ha forhøyet eCB i kroppen, f.eks. overvekt.

Med høyt nivå av n-6 relativt til n-3 blir det en overvekt av AA (arakidonsyre) som produserer en overvekt av eCB, som dermed fører til en reduksjon av eCB reseptorer. Dette gjør at smertestillende medikamenter fungerer dårligere, og at det blir lettere kronisk smerte. Tilskudd av n-3 gjør at eCB reseptorene øker. Studiene er gjort på mus og innebærer 17 g/kg.

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0089566

The endocannabinoid (eCB) system consists of receptors, endogenous ligands, and ligand metabolic enzymes. Metaphorically the eCB system represents a microcosm of psychoneuroimmunology or mind-body medicine. Cannabinoid receptor 1 (CB1) is the most abundant G protein-coupled receptor expressed in the brain, with particularly dense expression in (rank order): the substantia nigra, globus pallidus, hippocampus, cerebral cortex, putamen, caudate, cerebellum, and amygdala [1]. CB1 is also expressed in non-neuronal cells, such as adipocytes and hepatocytes, and in musculoskeletal tissues. Cannabinoid receptor 2 (CB2) is principally associated with cells governing immune function, although it may also be expressed in the central nervous [2], [3].

The eCB system’s salient homeostatic roles have been summarized as, “relax, eat, sleep, forget, and protect” [5]. It modulates embryological development, neural plasticity, neuroprotection, immunity and inflammation, apoptosis and carcinogenesis, pain and emotional memory, and most importantly from the viewpoint of recent drug development: hunger, feeding, and metabolism. Obese individuals seem to display an increased eCB tone, driving CB1activation in a chronic, feed-forward dysfunction (reviewed by [6]).

Other diseases are associated with suboptimal functioning of the eCB system. Russo [8]proposed that migraine, fibromyalgia, irritable bowel syndrome, and related conditions represent CEDS, “clinical endocannabinoid deficiency syndromes.” Fride [9] speculated that a dysfunctional eCB system in infants contributes to “failure to thrive” syndrome. Hill and Gorzalka [10] hypothesized that deficient eCB signaling could be involved in the pathogenesis of depressive illnesses. In human studies, eCB system deficiencies have been implicated in uncompensated schizophrenia [11], migraine [12], multiple sclerosis [13], Huntington’s [14],[15], uncompensated Parkinson’s [16], irritable bowel syndrome [17], uncompensated anorexia[18], and chronic motion sickness [19].

NSAIDs inhibit two cyclooxygenase (COX) enzymes, COX1 and COX2, and thereby block the conversion of arachidonic acid (AA) into inflammatory prostaglandins. Ibuprofen, ketorolac, and flurbiprofen also block the hydrolysis of AEA into arachidonic acid and ethanolamine [27]. SeeFigure 2. A binding site for some NSAIDs on FAAH has also been identified [28]. NSAID inhibition of COX2 blocks the metabolism of AEA and 2-AG into prostaglandin ethanolamides (PG-EAs) and prostaglandin glycerol esters (PG-GEs), respectively [29].

Combining NSAIDs with cannabinoids (either eCBs or exogenous cannabinoids) produces additive or synergistic effects. A sub-effective dose of WIN55,212-2 became fully antinociceptive following administration of indomethacin in rats [36].

In summary, preclinical studies indicate that some NSAIDs inhibit FAAH and enhance the activity of eCBs, phytocannabinoids, and synthetic cannabinoids. Combinational effects may be particularly relevant at peripheral sites, such as the peripheral terminals of nociceptors.

The distribution of glucocorticoid receptors (GRs) and CB1 overlap substantially in the central nervous system and other tissues, as do GRs and CB2 in immune cells. Dual activation of GRs and CBs may participate in glucocorticoid-mediated anti-inflammatory activity, immune suppression, insulin resistance, and acute psychoactive effects.

The acute administration of glucocorticoids may shift AA metabolism toward eCB synthesis in parts of the brain.

Chronic exposure to glucocorticoids downregulates the eCB system. Chronic corticosterone administration decreased CB1 densities in rat hippocampus [59] and mouse hippocampus and amygdala [61]. Chronic corticosterone administration in male rats led to visceral hyperalgesia in response to colorectal distension, accompanied by increased AEA, decreased CB1 expression, and increased TRPV1 expression in dorsal root ganglia. Co-treatment with the corticoid receptor antagonist RU-486 prevented these changes [62].

Polyunsaturated fatty acids (PUFAs) play fundamental roles in many cellular and multicellular processes, including inflammation, immunity, and neurotransmission. They must be obtained through diet, and a proper balance between omega-6 (ω-6) PUFAs and ω-3 PUFAs is essential. The typical Western diet contains a surfeit of ω-6s and a deficiency of ω-3s [130].

The inflammatory metabolites of AA are countered by dietary ω-3s. The two best-known ω-3s are eicosapentaenoic acid (EPA, 20:5ω-3) and docosahexaenoic acid (DHA, 22:6ω-3).

eCBs are derived from AA (see Figure 2). Several preclinical studies showed that dietary supplementation with AA increased serum levels of AEA and 2-AG, summarized in Table 1. Although we clearly need AA to biosynthesize eCBs, excessive levels of AA, administered chronically, may lead to excessive levels of eCBs. This in turn may lead to desensitized and downregulated CB1 and CB2 receptors.

Dietary supplementation with ω-3s predictably increased the concentration of EPA and/or DHA in tissues, cells, and plasma, and decreased the relative concentration of AA in tissues, cells, and plasma [132], [133]. ω-3 supplementation also decreased AEA and 2-AG in tissues, cells, and plasma (Table 1).

Adequate levels of dietary ω-3s are required for proper eCB signaling. Mice supplemented with ω-3s, compared to mice on a control diet, expressed greater levels of CB1 and CB2 mRNA.

n summary, dietary ω-3s seem to act as homeostatic regulators of the eCB system. In obese rodents fed a high-AA diet, ω-3s significantly decrease eCBs, especially 2-AG, particularly in tissues that become dysregulated, such as adipose and liver tissues. Plasma eCB levels are reduced by krill oil also in obese humans. Little change in eCB levels are seen in normo-weight individuals not fed a high ω-6 diet, and dietary ω-3s are required for proper eCB signaling.

Human intestinal epithelial cells incubated with L. acidophilus produced more CB2 mRNA [145]. Feeding L. acidophilus to mice and rats increased the expression of CB2 mRNA in colonic epithelial cells. Lastly, mice fed L. acidophilus showed less pain behavior following colonic distension with butyrate than control mice, an effect reversed by the CB2 antagonist AM630[145].

Chronic or repeated stress results in a chronic elevation of endogenous corticosterone via the hypothalamic-pituitary-adrenocortical (HPA) axis. Chronic stress (repeated restraint) reduced AEA levels throughout the corticolimbic stress circuit in rodents [99], [196], [197].

In summary, chronic stress impairs the eCB system, via decreased levels of AEA and 2-AG. Changes in CB1 expression are more labile. Stress management may reverse the effects of chronic stress on eCB signaling, although few studies exploring this possibility have been performed to date. Clinical anecdotes suggests that stress-reduction techniques, such as meditation, yoga, and deep breathing exercises impart mild cannabimimetic effects [218].

Massage and osteopathic manipulation of asymptomatic participants increased serum AEA 168% over pretreatment levels; mean OEA levels decreased 27%, and no changes occurred in 2-AG. Participants receiving sham manipulation showed no changes [218].

Upregulation of the eCB system in obese humans seems to be driven by excessive production of eCBs in several peripheral tissues such as visceral adipose tissue, liver, pancreas, and skeletal muscle.

In summary, increased food intake, adiposity, and elevated levels of AEA and 2-AG apparently spiral in a feed-forward mechanism. Weight loss from caloric restriction breaks the cycle, possibly by reducing CB1 expression and reducing eCB levels.

Although both types of exercise regimens increased eCB ligand concentrations, only long-term-forced exercise led to sustained elevations of eCBs, and predictable CB1 downregulation.

In whole animals, however, caffeine’s effects are biphasic and vary by dosage and acute versus chronic administration. In humans, the acute administration of caffeine decreases headache pain, but exposure to chronic high doses, ≥300 mg/day, may exacerbate chronic pain [275].

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

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Denne sier mye om nervenes blodgjennomstrømmning. Spesielt interessant er avnittet om hvor lite trykk som skal til før blodgjennomstrømningen stopper. Om trykket opprettholdes i 8 timer vil det skje en skade i nerven. Så lite som 20 mm Hg er nok til at blodsirkluasjonen blir dårligere.

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

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.

Arterial and endoneurial capillary blood flows were stopped at pressures of 50 to 70 mm Hg67 and 80 mm Hg,75 respectively. Interestingly, in humans, intraneural blood flow and sensory responses are blocked at extraneural tissue pressures 45 mm Hg below the mean arterial pressure.82 A compressive stress of only 30 mm Hg, if maintained for 2 hours, results in endoneurial edema,83 and, if maintained for 8 hours, results in endoneurial pressure high enough to subsequently impair blood flow.84 The endoneurial edema is thought to result from ischemic damage to endoneurial capillary endothelial cells and an alteration in the blood-nerve barrier. The same compressive stress of 30 mm Hg applied for 8 hours is sufficient to impair both anterograde axonal transport and retrograde axonal transport.85,86Increasing pressure results in greater tissue damage, as a compressive force of 150 mm Hg maintained for 30 minutes was shown to induce a degeneration of 30% of the distal fibers,48 and compressive forces of 200 and 400 mm Hg maintained for 2 hours were shown to block axonal transport for 1 and 3 days, respectively.87

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.