Forfatterarkiv: Marius

Ukjent sin avatar

Effectiveness of myofascial release: Systematic review of randomized controlled trials

av

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.

Ukjent sin avatar

Peripheral Nerve Entrapment and Injury in the Upper Extremity

av

Denne beskriver flere innklemningsnevropatier som kan oppstå i skuldre og armer.

Spesielt to prinsipper er smarte å ha med:

1: ved smerte eller svakhet i å løfte armen over hodet: suprascapular nerven

2: ved smerte eller svakhet i å skru inn en skrue: carpal tunnel eller pronator syndrom (median nerven)

http://www.aafp.org/afp/2010/0115/p147.html

Ukjent sin avatar

When pain is not only pain: Inserting needles into the body evokes distinct reward-related brain responses in the context of a treatment.

av

Denne beskriver hvordan smerte ikke alltid er smerte, at konteksten smerte gis i bestemmer hvordan det oppleves. Forklart med dry needling, så vil nåle-smerten være mindre smertefullt og oppleves positivt om det blir gitt i en kontekst som oppleves postivit vet at det er en del av behandlingsopplegget for å bli smertefri.

http://www.ncbi.nlm.nih.gov/pubmed/25528104

Abstract

The aim of this study was to compare behavioral and functional brain responses to the act of inserting needles into the body in two different contexts, treatment and stimulation, and to determine whether the behavioral and functional brain responses to a subsequent pain stimulus were also context dependent. Twenty-four participants were randomly divided into two groups: an acupuncture treatment (AT) group and an acupuncture stimulation (AS) group. Each participant received three different types of stimuli, consisting of tactile, acupuncture, and pain stimuli, and was given behavioral assessments during fMRI scanning. Although the applied stimuli were physically identical in both groups, the verbal instructions differed: participants in the AS group were primed to consider the acupuncture as a painful stimulus, whereas the participants in the AT group were told that the acupuncture was part of therapeutic treatment. Acupuncture yielded greater brain activation in reward-related brain areas (ventral striatum) of the brain in the AT group when compared to the AS group. Brain activation in response to pain stimuli was significantly attenuated in the bilateral secondary somatosensory cortex and the right dorsolateral prefrontal cortex after prior acupuncture needle stimulation in the AT group but not in the AS group. Inserting needles into the body in the context of treatment activated reward circuitries in the brain and modulated pain responses in the pain matrix. Our findings suggest that pain induced by therapeutic tools in the context of a treatment is modulated differently in the brain, demonstrating the power of context in medical practice.

Ukjent sin avatar

What is the evidence that neuropathic pain is present in chronic low back pain and soft tissue syndromes? An evidence-based structured review.

av

Denne beskriver hvordan det er en nevropatis komponent i nesten all kronisk ryggsmerte og mykvevsmerte.

http://www.ncbi.nlm.nih.gov/pubmed/24118776

In each grouping, 100% of the studies reported some prevalence of NP (none reported zero prevalence).

Ukjent sin avatar

The Enduring Impact of What Clinicians Say to People With Low Back Pain

av

Beskriver hvilken påvirkning ord har på pasienter. Spesielt når helsepersonell forteller at man på beskytte f.eks. ryggen ved ryggsmerter. Helsepersonells ideer om ryggsmerter smitter over på pasientene, derfor er det viktig at helsepersonell holder seg oppdatert på forskning, spesielt smerteforskning siden det er stort sett smerte folk kommer til behandling for.

http://www.annfammed.org/content/11/6/527.full

Many messages from clinicians were interpreted as meaning the back needed to be protected. These messages could result in increased vigilance, worry, guilt when adherence was inadequate, or frustration when protection strategies failed.

CONCLUSIONS Health care professionals have a considerable and enduring influence upon the attitudes and beliefs of people with low back pain. It is important that this opportunity is used to positively influence attitudes and beliefs.

Ukjent sin avatar

The magnitude of nocebo effects in pain: A meta-analysis

av

Denne viser atnocebo effekten er like stor som placebo effekten.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213146

The overall magnitude of the nocebo effect was moderate to large (lowest g = 0.62 (0.24-1.01) and highest g = 1.03 (0.63-1.43)) and highly variable (range of g = −0.43-4.05). The magnitudes and range of effect sizes was similar to those of placebo effects (d = 0.81) in mechanistic studies. In studies where nocebo effects were induced by a combination of verbal suggestions and conditioning, the effect size was larger (lowest g = 0.76 (0.39-1.14) and highest g = 1.17 (0.52-1.81)) than in studies where nocebo effects were induced by verbal suggestions alone (lowest g = 0.64 (−0.25-1.53) and highest g = 0.87 (0.40-1.34)). These findings are similar to those in the placebo literature. Since the magnitude of the nocebo effect is variable and sometimes large, this meta-analysis demonstrates the importance of minimizing nocebo effects in clinical practice.

Ukjent sin avatar

Chi is not energy

av

Denne artikkelen beskriver på svært godt vis hvordan konseptet chi beskrevet som energi blir misforstått som konseptet energi som vitenskapen forholder seg til. Forfatteren vil heller oversette «chi» til «effektivitet». Jo mer chi man har, jo mer effektivt fungerer kroppen.

http://taichiblog.spiralwise.co.uk/2011/09/chi-is-not-energy.html?m=1

The significance of what I’m saying is that in practical terms nothing changes. In our classes we can still «cultivate chi» (or «enhance efficiency»), and train in the same way we’ve been doing for centuries. Internally within our own bodies it feels as if we do have more energy (just as our new lightbulb will shine more brightly) and so we get that glow and feeling of health. However by reinterpreting chi as efficiencyrather than energy, the concept of chi is no longer at odds with Western science. There is no longer any discrepancy between Western science and Chinese medicine. The major obstacle of scepticism has been removed.

 

Ukjent sin avatar

Comparison of spinal fusion and nonoperative treatment in patients with chronic low back pain: long-term follow-up of three randomized controlled trials.

av

Denne nevner at 11 år etter en «spinal fusion» operasjon er det ingen forskjell på de som ble operert og de som ikke ble operert. De konkluderer med at «spinal fusion» ikke bør utføres så lenge det er andre muligheter for behandling tilgjengelig.

http://www.ncbi.nlm.nih.gov/pubmed/24200413

CONCLUSIONS:

After an average of 11 years follow-up, there was no difference in patient self-rated outcomes between fusion and multidisciplinary cognitive-behavioral and exercise rehabilitation for cLBP. The results suggest that, given the increased risks of surgery and the lack of deterioration in nonoperative outcomes over time, the use of lumbar fusion in cLBP patients should not be favored in health care systems where multidisciplinary cognitive-behavioral and exercise rehabilitation programmes are available.

Ukjent sin avatar

Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia

av

Beskriver hvordan magnesium mangel bidrar til økt utskillelse av Substans P i nociceptorer, som gir økt tilbøyelighet for smertetilstander. Den sier at det ikke holder meg bare magnesiumtilskudd, man må kombinere med antioksidanter også fordi magnesium mangel spiser opp antioksidantforsvaret. Den nevner at graden av magnesium mangel er nesten lineær med graden av Substans P aktivitet og antioksidant nedgang.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3753099/

This review has highlighted some key observations which helped formulate the hypothesis that release of substance P (SP) during experimental dietary Mg deficiency (MgD) may initiate a cascade of deleterious inflammatory, oxidative, and nitrosative events, which ultimately promote cardiomyopathy, in situ cardiac dysfunction, and myocardial intolerance to secondary stresses.

Significant protection against most of these MgD-mediated events has been observed with interventions that modulate neuronal SP release or its bioactivity, and with several antioxidants (vitamin E, probucol, epicaptopril, d-propranolol). In view of the clinical prevalence of hypomagnesemia, new treatments, beyond magnesium repletion, may be needed to diminish deleterious neurogenic and prooxidative components described in this article.

Animals placed on Mg-restricted diets also displayed progressive cardiovascular lesion formation, heightened cardiac inflammatory cell infiltration,15 decreased levels of endogenous antioxidants (glutathione, vitamin E, ascorbate) 16,17 and higher plasma levels of pro-oxidant metals 18 and lipid peroxidation (LPO) products.19,20 Antioxidant treatment attenuated the severity of both cardiovascular inflammation in vivo21 and postischemic reperfusion injury in vitro,22 suggesting that dietary Mg-deficiency progresses into a pro-oxidant condition.

The gut is rich in neuropeptides 53 and may contribute to the early rise in plasma SP during MgD. During week 1 of MgD, intestinal inflammation was evident and pronounced PMN infiltration occurred by week 3, when significant decreases in mucosal barrier function were observed.

Varying dietary Mg-intake in rats directly influenced plasma SP levels,58 the associated severity of systemic oxidative/nitrosative stress,59,60 and loss of myocardial tolerance to I/R stress. 58 We demonstrated that SP release also occurred in rats fed moderate MgD diets (MgD20 =20 % RDA; MgD40 = 40% RDA) 58 and the literature suggests that many of the same pathological characteristics observed in the severe MgD9 animal also occurred in these animals. 59,60

Moreover, the decline in RBC glutathione was also directly proportional to the extent of Mg-restriction: levels from MgD40, MgD20, and MgD9 rats fell 20.6%, 29.4%, and 50% compared to the Mg100 group.

 

 

Ukjent sin avatar

Cellular and Molecular Mechanisms of Pain

av

Denne beskriver det aller meste om nociceptorer. Jeg biter meg merke i det siste avsnittet som beskriver noe av årsaken til at det ikke er så enkelt som å kallen en nociceptor for smertereseptor. De avslutter med å si at studier av nocicepsjon kan bane vei for å forstå kronisk smerte, men av forrige blog jeg la ut forstår vi at i hjernen er det en tydelig forskjell mellom kronisk og akutt smerte. Så åpenbart er det helt andre mekanismer som ligger til grunn.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2852643/

These observations argue for behaviorally-relevant specificity at the level of the nociceptor. However, this is likely to be an oversimplification for at least two reasons. First, many nociceptors are polymodal and can therefore be activated by thermal, mechanical, or chemical stimuli, leaving one to wonder how elimination of large cohorts of nociceptors can have modality-specific effects. This argues for a substantial contribution of spinal circuits to the process whereby nociceptive signals are encoded into distinct pain modalities. Indeed, an important future goal is to better delineate neuronal subtypes within the dorsal horn and characterize their synaptic interactions with functionally or molecularly defined subpopulations of nociceptors. Second, the pain system shows a tremendous capacity for change, particularly in the setting of injury, raising questions about whether and how a labeled line system might accommodate such plasticity, and how alterations in such mechanisms underlie maladaptive changes that produce chronic pain. Indeed, we know that substance P-saporin-mediated deletion of a discrete population of lamina I dorsal horn neurons, which express the substance P receptor, can reduce both the thermal and mechanical pain hypersensitivity that occurs after tissue or nerve injury (Nichols et al., 1999). Such observations suggest that in the setting of injury specificity of the labeled line is not strictly maintained as information is transmitted to higher levels of the neuraxis.

Doing so should bring us closer to understanding how acute pain gives way to the maladaptive changes that produce chronic pain, and how this switch can be prevented or reversed.