Forfatterarkiv: Marius

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Inflammation-induced hyperalgesia: Effects of timing, dosage, and negative affect on somatic pain sensitivity in human experimental endotoxemia.

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En studie til som bekrefter at lav-grads betennelse gir hyperalgesi, altså økt smerteopplevelse.

http://www.ncbi.nlm.nih.gov/pubmed/24814500

Abstract

BACKGROUND:

Inflammation-induced pain amplification and hypersensitivity play a role in the pathophysiology of numerous clinical conditions. Experimental endotoxemia has recently been implemented as model to analyze immune-mediated processes in human pain. In this study, we aimed to analyze dose- and time-dependent effects of lipopolysaccharide (LPS) on clinically-relevant pain models for musculoskeletal and neuropathic pain as well as the interaction among LPS-induced changes in inflammatory markers, pain sensitivity and negative affect.

METHODS:

In this randomized, double-blind, placebo-controlled study, healthy male subjects received an intravenous injection of either a moderate dose of LPS (0.8ng/kg Escherichiacoli), low-dose LPS (0.4ng/kg), or saline (placebo control group). Pressure pain thresholds (PPT), mechanical pain sensitivity (MPS), and cold pain sensitivity (CP) were assessed before and 1, 3, and 6h post injection to assess time-dependent LPS effects on pain sensitivity. Plasma cytokines (TNF-α, IL-6, IL-8, IL-10) and state anxiety were repeatedly measured before, and 1, 2, 3, 4, and 6h after injection of LPS or placebo.

RESULTS:

LPS administration induced a systemic immune activation, reflected by significant increases in cytokine levels, body temperature, and negative mood with pronounced effects to the higher LPS dose. Significant decreases of PPTs were observed only 3h after injection of the moderate dose of LPS (0.8ng/kg). MPS and CP were not affected by LPS-induced immune activation. Correlation analyses revealed that decreased PPTs were associated with peak IL-6 increases and negative mood.

CONCLUSIONS:

Our results revealed widespread increases in musculoskeletal pain sensitivity in response to a moderate dose of LPS (0.8ng/kg), which correlate both with changes in IL-6 and negative mood. These data extend and refine existing knowledge about immune mechanisms mediating hyperalgesia with implications for the pathophysiology of chronic pain and neuropsychiatric conditions.

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Systemic Inflammation Decreases Pain Threshold in Humans In Vivo

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Denne viser hvordan systemisk betennelse, til og med lav-grads systemisk betennelse (som kommer fra kosthold), bidrar til å øke smertesensitivitet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3866228/

In conclusion, this study shows that systemic inflammation elicited by the administration of endotoxin to humans, results in lowering of the pain threshold measured by 3 quantitative sensory testing techniques. The current work provides additional evidence that systemic inflammation is accompanied by changes in pain perception.

Inflammation leads to a broad constellation of adaptive changes, called the ‘sickness response’. Features of this response include fever, increased sleep, decreased locomotion, decreased food and water intake, and hormonal changes [1]. Furthermore, the pain threshold for painful stimuli is lowered, resulting in hyperalgesia, and normally non-painful stimuli can become painful (allodynia).

Systemic inflammation has previously been shown to alter pain perception in animals and humans. Recently, Benson and colleagues reported altered pain perception after the administration of a very low dose of endotoxin (0.4 ng/kg) to healthy volunteers, mimicking low grade systemic inflammation [26].

 

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Hyperglycemia enhances the cytokine production and oxidative responses to a low but not high dose of endotoxin in rats.

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Denne beskriver hvordan hyperglycemi (regnes som blodsukker over 7 mmol/L i lengre perioder, eller fastende blodsukker over 7) gir økt cytokin-aktivitet i flere timer etter en stressende episode. Om man spiser en snickers går blodsukkeret opp til over 10, og om man kontinuerlig spiser mat som øker blodsukkeret er det en stor sjangse for at man har en kronisk betennelsesreaskjon med økt cytokin aktivitet.

Kobler vi det med denne, som nevner at cytokiner tilført fra utenfor muskelen kan gi hyperalgesi, så begynner bildet å bli klarere: «One mechanism of action, the immune-to-brain communication through activation of brain and spinal cord glial cells was reviewed by Wieseler-Frank et al. (2005). Activation of CNS glia and subsequent production of inflammatory cytokines can lead to hyperalgesia.» http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1552097/

Abstract

OBJECTIVE:

The aim of this study was to investigate whether hyperglycemia enhances the systemic inflammatory response and oxidative stress induced by endotoxin.

DESIGN:

Laboratory investigation.

SETTING:

University medical school.

SUBJECTS:

Forty-one male Sprague-Dawley rats.

INTERVENTIONS:

A hyperglycemic condition was produced in rats by glucose clamp for 3 hrs. Immediately on stopping the glucose infusion, animals received different doses of endotoxin injection (0, 0.2, or 1 mg/kg), and then blood glucose concentration was monitored over the ensuing 2 hrs. At the end of 2 hrs, levels of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, corticosterone, and alpha-1 acid glycoprotein were determined in serum, and malondialdehyde and total glutathione content were determined in the liver.

MEASUREMENTS AND MAIN RESULTS:

Over the 2-hr period, blood glucose concentrations returned to normal in initially hyperglycemic rats. However, the levels of cytokines, corticosterone, and alpha-1 acid glycoprotein were significantly higher in these animals compared with nonhyperglycemic controls, demonstrating an extended effect of prior hyperglycemia on markers of systemic inflammation. With low-dose (0.2 mg/kg) but not high-dose (1 mg/kg) endotoxin administration, hyperglycemic animals had significantly higher levels of cytokines compared with controls, indicating that prior hyperglycemia can enhance the systemic inflammatory response to a moderate endotoxin dose, but that the maximum effects of endotoxin on production of inflammatory cytokines are not altered by transient high glucose exposure.

CONCLUSIONS:

Systemic inflammation persists for a period following hyperglycemia, and this can enhance the systemic inflammatory response to a subsequent moderate stress.

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Noen studier om hvordan Substans P forholder seg til mat

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Denne nevner at en 10% reduksjon av anbefalt daglig magnesium inntakt øker sjangsen for osteoporose og Substans P

Bone Loss Induced by Dietary Magnesium Reduction to 10% of the Nutrient Requirement in Rats Is Associated with Increased Release of Substance P and Tumor Necrosis Factor-α1 

http://jn.nutrition.org/content/134/1/79.long

These data demonstrated that a Mg intake of 10% of NR in rats causes bone loss that may be secondary to the increased release of substance P and TNF-α.

Denne nevner hvordan tiltak som reduserer SP bidrar til å redusere de negative virkningene av magnesiummangel.

Neurogenic Inflammation and Cardiac Dysfunction due to Hypomagnesemia.

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

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.

Denne nevner hvordan SP er involvert i insulin regulering og diabetes.

Role of Substance P in the Regulation of Glucose Metabolism via Insulin Signaling-Associated Pathways

 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230056/

Our results demonstrate an important role for SP in adipose tissue responses and obesity-associated pathologies. These novel SP effects on molecules that enhance insulin resistance at the adipocyte level may reflect an important role for this peptide in the pathophysiology of type 2 diabetes.

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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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Focal vibration in neurorehabilitation.

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Studien som går igjennom det meste av studier på hvordan vibrasjon påvirker nervesystemet og forskjellige sykdommer. Denne nevner bare rask vibrasjon, fra 60Hz og oppover. Konklusjonen er at vibrasjonsbehandling er en trygg, uten bivirkninger, lett å bruke og behagelig for klienten. Den bidrar med å redusere spastisitet (muskelsammentrekning), øker motorisk aktivitet (som bevegelse og balanse), og øker evnen til motorisk opplæring (f.eks. å gå etter en slagepisode).

http://www.ncbi.nlm.nih.gov/pubmed/24842220

Hele her: http://www.minervamedica.it/en/getfreepdf/rOWy4PI4QqWESC28Sd%252B0UzVdpsQOpf0m1DjcPEUPxCXxOj8vi44aZEOle9uSoxBxdhfWcbrG8imEfQUEkQLrCw%253D%253D/R33Y2014N02A0231.pdf

Abstract

During the last decade, many studies have been carried out to understand the effects of focal vibratory stimuli at various levels of the central nervous system and to study pathophysiological mechanisms of neurological disorders as well as the therapeutic effects of focal vibration in neurorehabilitation. This review aimed to describe the effects of focal vibratory stimuli in neurorehabilitation including the neurological diseases or disorders like stroke, spinal cord injury, multiple sclerosis, Parkinson’s’ disease and dystonia. In conclusion, focal vibration stimulation is well tolerated, effective and easy to use, and it could be used to reduce spasticity, to promote motor activity and motor learning within a functional activity, even in gait training, independent from etiology of neurological pathology. Further studies are needed in the future well-designed trials with bigger sample size to determine the most effective frequency, amplitude and duration of vibration application in the neurorehabilitation.

 

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To studier på smertestillende effekt av Percussor

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To studier forklarer det mye om hvordan percussorbehandling reduserer smerte, og bekrefter mine teorier som er beskrevet i artikkelen om Percussor behanding. Nevner at nerver i huden skaper en interaksjon mellom de to områdene av hjernen som involverer smerte og berøring. Distraksjon sier de ikke er en del av den smertereduserende effekten.

How does vibration reduce pain?

http://www.ncbi.nlm.nih.gov/pubmed/24689133

Abstract

Cutaneous vibration is able to reduce both clinical and experimental pain, an effect called vibratory analgesia. The traditional explanation for this phenomenon is that it is mediated by lateral inhibition at the segmental (spinal cord) level, in pain-coding cells with center-surround receptive fields. We evaluated this hypothesis by testing for two signs of lateral inhibition-namely (1) an effect of the distance between the noxious and vibratory stimuli and (2) an inhibition-induced shift in the perceived location of the noxious stimulus. The experiment involved continuous ratings of the pain from pressure applied to the back of a finger, alone and in the presence of vibration delivered to sites on the palm of the hand both near to and far from the site of painful stimulation. Neither prediction of the segmental hypothesis was supported. There was also little evidence to support the view (widely held by subjects) that distraction is the primary mechanism of vibratory analgesia. The results are more consistent with a recently proposed theory of interactions between two cortical areas that are primarily involved in coding pain and touch, respectively.

Vibratory antinociception: effects of vibration amplitude and frequency.http://www.ncbi.nlm.nih.gov/pubmed/14622680

Abstract

The ability of cutaneous vibration to compromise detection of a nociceptive stimulus was examined in 2 sets of psychophysical experiments. The noxious stimulus was a 10-millisecond burst of radiant heat from a CO2 laser; at the near-threshold levels used it generally yielded a mild pricking sensation. In both experiments, the detectability (de′) of the laser was measured in the presence of different vibratory stimuli and in the absence of vibration. Periods of vibration lasted 10 seconds, bracketing the time of occurrence of the laser. Vibratory and laser stimuli were presented 2.3 cm apart on the dorsal surface of the forearm. Confidence rating procedures yielded receiver operating characteristic curves from which detectability of the laser was calculated. In an amplitude study, vibrations ranging from 10 to 45 dB above threshold were used; results indicated that nociceptive sensitivity gradually declined as vibration amplitude increased. In a frequency study, vibrations ranging from 20 to 230 Hz were used; all interfered with nociception. Combining the results of the 2 studies permitted the conclusion that signals in multiple vibrotactile channels are able to modulate nociception. No one mechanoreceptive channel appears to have a privileged role.

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Oxygen regulation and limitation to cellular respiration in mouse skeletal muscle in vivo

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Denen Studien sier noe ekstremt viktig: Oksygen, mye eller lite, har ingen ting med regulering av cellerespirasjon å gjøre annet enn å være tilgjengelig som et substrat (altså noe cellene kan leve på). De nevner at oksygen bare blir et problem om det går under 2-3 mmHg. Og at blodceller virker som enn buffer ved at de slipper av oxygen for å holde det ovenfor

Marcinek et.al. 2003. Oxygen regulation and limitation to cellular respiration in mouse skeletal muscle in vivo.

http://ajpheart.physiology.org/content/285/5/H1900.full

Therefore, we reject a regulatory role for oxygen in cellular respiration and conclude that oxygen acts as a simple substrate for respiration under physiological conditions.

LOW OXYGEN TENSIONS are characteristic of active muscle. During maximal aerobic exercise, intracellular PO2 in skeletal muscle falls to as low as 2–3 mmHg based on an average myoglobin (Mb) saturation of ∼50% (24, 27). The intracellular oxygen tension at the maximal rate of sustained exercise sets the lower end of the range of physiologically relevant intracellular PO2 values. These values are just above the threshold where isolated mitochondria (12,29), isolated cells (39, 40), and intact muscle (28) begin to become oxygen limited. Thus the intracellular PO2 reached during heavy muscle exercise may approach the threshold for limiting cellular respiration in vivo.

Experiments in isolated mitochondria and cells have shown that the respiration rate remains relatively constant over the physiological PO2 range (12, 36), with a clear reduction occurring only at PO2 below 2–3 mmHg.

Our in vivo results from the mouse hindlimb indicate that until a threshold PO2 is reached (2–3 mmHg), there is no effect of oxygen tension on the phosphorylation state of the cell.

In mouse skeletal muscle in vivo, oxygen tension in the physiological range had no significant effect on cellular respiration over a threefold range of baseline rates of oxygen consumption. This is the expected outcome if oxygen is acting as a simple substrate with no significant regulatory role under physiological conditions.

Thus we found no evidence for a change in the relationship between respiration rate and intracellular PO2 with a greater than threefold increase in the fully oxygenated respiration rate. This leads us to conclude that oxygen is not limiting to cellular oxygen consumption and, therefore, does not play a significant role in regulating cellular respiration in vivo under these conditions.

Studies on exercising human muscle support the conclusion that oxygen tension in skeletal muscle does not fall to levels low enough to significantly inhibit cellular respiration except under extreme physiological conditions [i.e., maximum oxygen consumption (V̇O2 max) in trained individuals]. These studies indicate that Mb saturations at the aerobic capacity of human skeletal muscle are ∼50% in vivo (2.4 mmHg) (24, 27). Our results indicate that above this intracellular PO2, there is little effect of oxygen tension on the cellular respiration rate over the range tested in the present study.

Decreasing the capacity for oxygen delivery by breathing hypoxic air was found to drop Mb saturation below the 50% level and to reduce oxygen consumption during exercise (26). In contrast, supplementing oxygen by breathing of hyperoxic air during a maximum oxygen consumption test either did not effect or resulted in a small increase (∼10%) in V̇O2 max (6, 25).

The transition between oxygen-independent and oxygen-dependent respiration in vivo also occurs in this range of intracellular oxygen tensions (2–3 mmHg). Therefore, an important role of Mb in skeletal muscle may be as an oxygen buffer to help maintain intracellular PO2 above the point at which it becomes limiting to cellular respiration.

In conclusion, the findings of the present study lead us to reject the hypothesis that oxygen plays a regulatory role in cellular respiration over the physiological range of intracellular oxygen tensions. This conclusion is based on the absence of interaction between [PCr], pH (and therefore phosphorylation state), oxygen consumption, and PO2 above 3 mmHg over a greater than threefold range in oxygen consumption rates. These results are consistent with the hypothesis that oxygen acts as a simple substrate for cellular respiration over the physiological range of oxygen tensions.

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Psychosocial factors in the workplace–do they predict new episodes of low back pain? Evidence from the South Manchester Back Pain Study.

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Studie fra 1997 som forteller at å være misfornøyd med arbeidssituasjonen sin gir dobbelt så stor sjangse for ryggsmerter enn om man er fornøyd med arbeindssituasjonen.

http://www.ncbi.nlm.nih.gov/pubmed/9160473/

Abstract

STUDY DESIGN:

A prospective, population-based cohort study of working adults.

OBJECTIVES:

To determine whether work-related psychosocial factors and social status predict the occurrence of new episodes of low back pain and influence consultation behavior.

SUMMARY AND BACKGROUND DATA:

Dissatisfaction with work and social status has been associated with low back pain in several studies; few of these studies have been prospective or population based.

METHODS:

An initial postal survey was returned by 4,501 (59%) adults (18-75 years old) registered with two primary care practices. From this, a cohort of 1,412 people currently in employment and free of low back pain was identified, and baseline information on work-related psychosocial factors and psychologic distress was obtained. Social class was derived from current occupation using a standardized classification. New episodes of low back pain occurring in the next 12 months were identified by continuous monitoring of primary care consulters and by mailing a second questionnaire a year later to identify occurrences of low back pain for which no consultation was sought.

RESULTS:

The baseline cross-sectional survey showed modest but significant associations between low back pain and perceived inadequacy of income (risk ratio 1.3), dissatisfaction with work (risk ratio 1.4) and social class IV/V (risk ratio 1.2). In the follow-up year, the risk of reporting low back pain for which no consultation was sought doubled in those dissatisfied with their work. Both perceived inadequacy of income (odds ratio 3.6) and social class IV/V (odds ratio 4.8) were strongly associated with consulting with a new episode of low back pain during the follow-up year, an association more marked in women. The associations with work dissatisfaction and perceived adequacy of income were not explained by general psychologic distress or social status.

CONCLUSION:

People dissatisfied with work are more likely to report low back pain for which they do not consult a physician, whereas lower social status and perceived inadequacy of income are independent risks for working people to seek consultation because of low back pain.