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

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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.

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

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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).

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

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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.

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

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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.

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

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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.

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Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia

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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.

 

 

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Cellular and Molecular Mechanisms of Pain

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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.

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Human brain mechanisms of pain perception and regulation in health and disease

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Denne beskriver det meste rundt hvordan forskjellige områder av hjernen aktiveres i smertetilstander.

Klikk for å få tilgang til NP%20-%20Apkarian%20-%202005%20-%20Human%20brain%20mechanisms%20of%20pain%20perception.pdf

 

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.

 

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The conundrum of sensitization when recording from nociceptors

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Mer fra Geoffrey Bove om nervogene betenneler og nocicepsjon. Denne forholder seg til nocicepsjon som oppstår under måling av nocicepsjon i studier, men har mange interessante poenger. Nevner at noceceptiv sensitering og kontinuerlig nociceptive aktivitet (ongoing activity(OA)) skjer spesielt i betennelsestilstander. Dette er grunnen til at alle med betennelsestilstander i kroppen bør senke betennelsesnivå for å få resultater av behandling.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854223/

When sensitized, nociceptors often exhibit activity in the absence of apparent or additional stimulation, called ongoing (or spontaneous) activity (OA).

We suggest that there are two types of OA, characterized by their rates. Very slow rates of ongoing activity (<0.2 Hz) are likely to arise from the receptive field and may indicate sensitization during the experiment. Faster rates are likely to arise from the nerve trunk, i.e. the neuritis, or the neuronal cell body.

A key feature of nociceptors is that they develop ongoing activity (OA) when they, or the structures they innervate, are injured or inflamed (Bessou and Perl, 1969; Perl, 1976; Perl, Kumazawa et al., 1976).

To locate RFs, especially in deep tissues, the structures must be stimulated noxiously. Thus, when a slowly conducting neuron is isolated, the peripheral structures from the distal thigh to the toes are stimulated noxiously using fingers or forceps. However, if a mechanical receptive field is not found, another neuron is isolated, and the search repeated. This typically takes dozens of searches over the course of the recording sessions, which in these experiments were 4–7 hours long. In our experiments it was clear that the noxious mechanical stimulus necessary to identify the RFs was in itself sufficient to cause inflammation.

Ongoing activity in sensory elements could be expected to impact the sensory modality of that element. Thus, OA in nociceptors could be expected to lead to the sensation of pain. However, the discharge rate that is necessary to reach perception remains unclear, and definitive studies have not been performed.

Using microneurography in humans, which is similar to the methods reported here, Konietzny et al., reported that electrically evoked nociceptor discharge rates as low at 0.5 Hz could evoke pain (Konietzny, Perl et al., 1981). Another human study reported that while nociceptor discharge under 0.2 Hz usually did not evoke pain, 0.4 Hz usually did (Van Hees and Gybels, 1981), consistent with a similar report (Van Hees and Gybels, 1972). These findings are in general consistent with our findings (Fig. 3). Although it thus remains unknown whether very slow levels of OA are significant for pain, any low rate will release neurotransmitters at their synapses in the spinal cord, which may be extensive due to the high degree of branching of primary afferent neurons to spinal cord neurons.

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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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