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
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
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.
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).
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.
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.
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.
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
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.
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.
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.
Denne beskriver det meste rundt hvordan forskjellige områder av hjernen aktiveres i smertetilstander.
Both primary somatosensory cortex (S1) and secondary somatosensory cortex (S2) are commonly activated in heat pain studies. Evidence suggests that the nociceptive input into these regions at least partially underlies the perception of sensory fea- tures of pain (Coghill et al., 1999; Peyron et al., 1999; Bushnell et al., 1999; Chen et al., 2002). Anterior cingu- late (ACC) and insular (IC) cortices, both components of the limbic system, are activated during the majority of PET or fMRI studies of heat pain, and these regions have been implicated in the affective processing of pain (Rainville et al., 1997; Tolle et al., 1999; Fulbright et al., 2001). Prefrontal cortical areas, as well as parietal association areas, are also sometimes activated by heat pain and may be related to cognitive variables, such as memory or stimulus evaluation (Coghill et al., 1999; Strigo et al., 2003). Motor and pre-motor cortical areas are on occasion activated by heat pain, but these activa- tions are less reliable, suggesting they may be related to pain epiphenomena, such as suppression of movement or actual pain-evoked movements themselves.
Subcortical activations are also observed, most notably in thalamus (Th), basal ganglia, and cerebellum (eTable 1). Fig. 1 illustrates the brain regions most com- monly reported activated in pain studies.
Utilizing similar methodology, rCBF responses to a l-opioid agonist, remifentanil, were com- pared to that elicited by a placebo (Petrovic et al., 2002a). The two effects overlapped in terms of rCBF increases in dorsal ACC, suggesting that this brain region may be in- volved in placebo effects. Perhaps more notably, placebo responders showed responses to remifentanil that were more prominent than non-responders. These data suggest that the placebo effect on pain responses may be mediated by inter-individual variations in the ability to activate this neurotransmitter system, as hypothesized by others (Amanzio and Benedetti, 1999).
Another recent study demonstrated that thermal stimulation in com- plex regional pain syndrome (CRPS) patients gives rise to activity that closely matches that observed in normal subjects. However, this pattern changes dramatically when the ongoing pain of CRPS is isolated, by com- paring brain activity before and after sympathetic blocks that reduce the ongoing CRPS pain but do not change the thermal stimulus pain (Apkarian et al., 2001). Thus, there is no compelling evidence that examining brain responses to experimental painful stimuli can predict the pattern of brain responses in chronic clinical pain states.
Thus, we can assert that brain activity for pain in chronic clinical conditions is different from brain activity for acute painful stimuli in normal subjects. We add the caution that this does not imply that all clinical pain conditions have a homo- geneous underlying brain activity pattern. On the con- trary, most likely the patterns involving different clinical conditions are unique but with the current avail- able data we cannot test this at a meta-analysis level.
The brain imaging studies reviewed here indicate the cortical and sub-cortical substrate that underlies pain perception. Instead of locating a singular ‘‘pain center’’ in the brain, neuroimaging studies identify a network of somatosensory (S1, S2, IC), limbic (IC, ACC) and asso- ciative (PFC) structures receiving parallel inputs from multiple nociceptive pathways (Fig. 1). In contrast to touch, pain invokes an early activation of S2 and IC that may play a prominent role in sensory-discriminative functions of pain. The strong affective-motivational character of pain is exemplified by the participation of regions of the cingulate gyrus. The intensity and affec- tive quality of perceived pain is the net result of the interaction between ascending nociceptive inputs and antinociceptive controls. Dysregulations in the function of these networks may underlie vulnerability factors for the development of chronic pain and comorbid conditions.
Our analysis, in- stead, suggests that chronic pain conditions may be a reflection of decreased sensory processing and enhanced emotional/cognitive processing.
Verkstedet Bodywork & Breathing System 