Er ett spm nok?

Depresjon og angst er sterke indikatorer for hvor god prognose man har på å bli frisk fra smerter. Har man depresjon er sjangsen større for at smertene vedvarer. For behandlere er det nok å stille ett (eller to) spørsmål for å avklare dette.

Spørsmålene er:

“have you been affected by sadness/depression during the last month” and “have you been affected by anxiety during the last month”

http://www.bodyinmind.org/is-one-question-enough-to-screen-for-depression-and-anxiety/

Om diafragma – hovedpustemuskelen

Om diafragma

Rett nedenfor lungene sitter vår hovedpustemuskel: diafragma.

Det er en svært sterk muskel. Sammen med hjertet, som er en stor klump med sterke muskelceller, er diafragma en muskel som går og går, dag og natt, hele livet. Fra du er foster i magen bare noen uker gammel, til du trekker ditt siste åndedrag. Man skulle tro diafragma var en sterk og tykk muskel, så mye og så hardt som den jobber. Men overraskende nok er diafragma en svært tynn muskel. Om vi tar den ut kan vi se tvers igjennom den.

For de fleste i vår kultur som jobber på kontor, stresser hver dag og hyperventilerer, blir diafragma muskelen, hovedpustemuskelen, lite brukt. Fremoverbøyd holdning, spente nakkemuskler, stive hofter, stiv korsrygg, m.m., blokkerer diafragmas bevegelse og over tid blir muskelen svak og lite bevegelig.

Et av de viktigste bidragene VBS har er øvelser for å styrke diafragma muskelen og øke den bevegelsesutslag. Du får større lungevolum, sterkere og stødigere pustefunksjon, og bedre holdning.

Den primære pustemuskelen i hvile er diafragma. Ved optimal pust er det kun diafragma som er aktiv i innpusten, mens alle andre muskler i brystkassen er helt avslappet. Ved en uanstrengt pust er det ingen bevegelse i brystkassen i det heletatt. Diafragma er en del av kroppens kjernemuskulatur og har en administrerende funksjon i stabilitet og tonus.

Rundt brystkassen har vi også mange tilleggspustemuskler vi kan bruke ved behov. Spesielt i mellom hvert ribbein, i skuldrene og i nakken. Om disse muskelene brukes når vi hviler er det et tydelig tegn på at pusten ikke fungerer optimalt, med tilhørende ugunstig holdning:

  • forward head posture
  • innoverroterte skuldre og utstående skulderblader
  • en rigid brystkasse og avstivet ryggrad

Vi får en lang kjede av problemer:

  • hodepine, nakke- og ryggsmerter, muskelspenninger
  • skuldersmerter, lite bevegelighet og lett for skader og leddbetenneler.
  • kjeve- og ansiktsspenninger
  • dårligere fordøyelse
  • ustabil hjerterytme, høyt blodtrykk
  • mindre lungekapasitet

Mange kaller diafragma for kroppens kongemuskel fordi den har en finger med i absolutt alt som skjer både internt kjemisk med oksygen- og energimetabolisme, og eksternt i bevegelse av både rygg, armer og bein, i tillegg til å påvirke holdningen i ryggraden og brystkassen.

Når vi trekker pusten inn går diafragma nedover for å utvide lungene. Når vi puster ut går diafragma oppover fordi lungene blir mindre.

Diafragma er kuppelformet slik at når den trekker seg sammen blir den flatere og bredere. Vi kan se dette når den nederste delen av brystkassen utvider seg på innpust og trekker seg sammen på utpust.

Innpusten krever en sterk diafragma for å utvide lungene, mens utpusten kan være helt passiv. I utpusten vil lungenes elastiske vev gjøre at de trekker seg sammen igjen og dytter luften ut, uten at vi trenger å bruke noen krefter på det. Kun om vi ønsker å utvide lungekapasiteten, for å tømme det man kaller «dead space», trenger vi å bruke krefter på utpust.

I tillegg til diafragma er mange muskler både imellom ribbeina, opp i nakken og ned i magen også med som sekundære pustemuskler når det trengs. Disse er med på å utvide lungene i alle retninger når vi trenger ekstra lungekapsitet.

Når vi puster med magen bruker vi diafragma mer enn når vi puster med toppen. Men med maksimal magepust blir det et positivit trykk i mageregionen som stopper diafragma bevegelse mot slutten av innpusten. Dette trykket er årsaken til at gravide får pusteproblemer mot slutten av svangerskapet. Diafragma får ikke beveget seg nok på innpusten.

For full utnyttelse og opptrening av diafragma-muskelen kan vi gjøre noen smarte grep.

For det første trekker vi navlen litt inn mot ryggraden og spenner av magemusklene. Dette gjør at vi får undertrykk i mageregionen slik at diafragma kan bevege seg maksimalt nedover på innpust.

For det andre kan vi strekke brystkassen litt oppover slik at baksiden av diafragma kan få maksimal vandring nedover mot nyrene.

Og for det tredje, på utpusten kan vi trekke navlen enda mer inn mot ryggraden for å skape et positivt trykk i mageregionen som er med på å dytte diafragma og lungene oppover.

Diafragma har muligheten til å bevege seg hele 10 cm opp og ned inni kroppen. Og siden den er koblet til alle indre organer, som hjerte, lever, nyrer, tarmer og ryggrad, kan en slik diafragmisk pust massere hele kroppen fra innsiden. Hjertet kan bevege seg 7 cm opp og ned sammen med diafragma. Lever 3 cm. Nyrer 5 cm. Ryggraden trekker seg sammen på innpust og strekker seg ut på utpust med hele 1-2 cm som et trekkspill.

Når du puster med topp-pust i lang tid så blir store deler av lungene ubrukt. Går det lang nok tid så vil bindevev stramme seg og gjøre at selv om vi puster maksimalt inn så får vi opplevelsen av å ikke få inn nok luft. Men heldigvis har menneskekroppen en kontinuerlig regenereringsmekanisme, så om vi gjør øvelsene våre, gir kroppen riktig næring og riktig trening, så kan selv lukkede og ødelagte deler av lungene reparere seg.

Sleep apnea may offer unusual protection for heart attack patients

Denne artikkelen nevner forskning som viser at «intermittent hypercapnia» (metabolsk pust) aktiverer mekanismer som øker produksjonen av nye blodkar. For de med søvnapne kan pustepausene faktisk være en beskyttelsesmekanisme og gjøre at de tåler bedre et eventuelt hjerteattakk.

http://www.sciencedaily.com/releases/2013/01/130102161108.htm

Her er selve studien: http://www.ncbi.nlm.nih.gov/pubmed/23155141

Og en kommentar som forteller at det ikke bare er så enkelt: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3570643/

Blood samples drawn from these patients revealed that the sleep disordered breathing patients had markedly higher levels of endothelial progenitor cells (EPCs), which give rise to new blood vessels and repair the injured heart, than the healthy sleepers. They also had higher levels of other growth-promoting proteins and immune cells that stimulate blood vessel production.

«Indeed, our results point at the possibility that inducing mild-moderate intermittent hypoxia may have beneficial effects,» Lena Lavie said.

Dry Needling Related Short-Term Vasodilation in Chronic Sciatica under Infrared Thermovision

Denne viser med bilder at blodsirkulasjonen økes i samme mønster som strålingsymtpomer fra musklene. I denne forbindelse ser de på dry needling av gluteus minimus hos de med ischas-symptomer. De som ikke fikk strålingssymptomer fikk heller ikke økt blodsirkulasjon, som vist i de nederste to radene i bildet.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4363707/

Conclusion. GM active TrPs prevalence among chronic sciatica patients was around one in three. Every TrPs-positive subject presented with vasodilatation under IRT in the area of DN related referred pain. Although TrPs involvement in chronic sciatica patients is possible, further studies on a bigger group of patients are still required.

Learning mechanisms in pain chronification—teachings from placebo research

Denne beskriver hvordan placebo-forskning bidrar til forståelsen av overgangen fra akutt smerte til kronisk smerte. Mange interessante prinsipper å få med seg her. Bl.a. årsaken til at det ikke er mulig å kile seg selv.

http://journals.lww.com/pain/Fulltext/2015/04001/Learning_mechanisms_in_pain.4.aspx

Abstract: This review presents a general model for the understanding of pain, placebo, and chronification of pain in the framework of cognitive neuroscience. The concept of a computational cost-function underlying the functional imaging responses to placebo manipulations is put forward and demonstrated to be compatible with the placebo literature including data that demonstrate that placebo responses as seen on the behavioural level may be elicited on all levels of the neuroaxis. In the same vein, chronification of pain is discussed as a consequence of brain mechanisms for learning and expectation. Further studies are necessary on the reversal of chronic pain given the weak effects of treatment but also due to alarming findings that suggest morphological changes in the brain pain regulatory systems concurrent with the chronification process. The burden of chronic pain is devastating both on the individual level and society level and affects more than one-quarter of the world’s population. Women are greatly overrepresented in patients with chronic pain. Hence, both from a general standpoint and from reasons of health equity, it is of essence to advance research and care efforts. Success in these efforts will only be granted with better theoretical concepts of chronic pain mechanisms that maps into the framework of cognitive neuroscience.

The seminal article of Craig with the description of pain as a homoeostatic emotion12 moved the field away from the concept of a “searching for pain center” in the brain to a systems-oriented understanding. The experience of pain was put in a behavioural perspective and the dynamics of the preprogrammed complex emotional reactions to acute pain were explained in terms of a dynamic regulatory system. Just as in all other expressions of emotion, the homoeostasis model for understanding pain provides both a basis for a prolongation of the feeling state but also, at the same time, an effective measure of social communication to alert others of, eg, danger. In addition, such a mechanism also serves to raise empathic responses in the group. The understanding of pain as a homoeostatic emotion has also contributed to the understanding of affective comorbidity in different pain syndromes because the mechanisms of both lowered mood and anxiety are based on similar regulatory mechanisms.53

Increasingly, the view on the brain function as a machinery for predictions has gained support. We and others have pointed out that this also is an important principle in pain perception and regulation and especially for the subjective reporting of pain.

Predictions entail the ability to internally maintain models of the world and to constantly update those with sparse multisource bits of information, principles that have been well established in sensory-motor learning.52 In short, upon an execution of a movement, an efferent copy is made as to serve as an internal model for the coming sensory feedback. This minimises the need for further computations as only discrepancies between the inner model and the received sensory feedback is ground for corrective behaviour, whereas expected input may be blocked from entering the motor-planning system. This understanding also explains why it is impossible to tickle oneself.6

Also, Kurzweil’s suggestion for the construction of the cortical architecture satisfies the needs for a multilevel system in which Bayesian principles for model optimisation can be harboured.27 The Bayesian principles posit that all current information is related to prior beliefs (ie, predictions).

We have left the era when the debate focused on whether a placebo effect is real or not.46 When placebo is understood in the context of dynamic complexity, that debate becomes redundant. Any notion that placebo would be constantly present and thus remains constant over time is incorrect because placebo rests on the discrepancy between the inner representational model and the current information inflow. If such a discrepancy remains over time, the inner model will update, and with the diminishing computational difference, and the placebo effect will disappear with time.

The ultimate difference in such a comparison system is of course if the expectation is no input but instead a sensory input is evoked as a surprise. In such situations with low predictability, the subjective experience of nociception seems to amplify.45

An insulin based model to explain changes and interactions in human breath-holding.

Her er et nytt stikk i siden for «oksygen Illusjonen».

I denne studien viser de hvordan «the breakpoint», altså det punktet hvor man ikke greier å holde pusten lenger, ikke har noen assosiasjon med oksygen. Det har assosiasjon med insulin!

Når vi holder pusten og oksygennivået synker, begynner kroppen etterhver å skape energi av sukker. Da økes insulinbehovet. Etter en stund brukes insulinet opp, og først da (!!!) trenger kroppen å puste inn får å få energi fra oksygen igjen.

Oksygen har veldig lite med saken (cellerespirasjon) å gjøre annet enn som en lett tilgjengelig og utømmelig energikilde. Det er interessant å legge merke til at diabetikere, som har lite insulin, har også svært vanskelig for å holde pusten.

Forfatterene beskriver også hvordan trening av diafragma gir evnen til å holde pusten lenger. Og de forklarer hvilke nevrologiske problemer man kan få av å ignorere kroppens signaler om å puste inn, slik konkurransedykkere gjør.

De nevner at vagus nerven reduserer insulin utskillelse. På innpust aktiveres vagus´ afferente (opp til hjernen) signaler pga strekk-reseptorer i lungene, som skrur av innpust-delen av hjernen slik at utpust kan starte (Hering-Breuer reflex). I innpust er det ikke behov for insulin fordi det er nok oksygen tilgjengelig. Derfor gir innpust en stimuli som reduserer insulinutskillelse. Men når man er i innpust-modus i lang tid og opplever hypoxi, vil oksidativt stress virke som et insulin-økende signal. Insulin stimulerer carotid-receptorene, som videre stimulerer hjernen til å aktivere innpust.

Insulin, sammen med kortikosteroider (stresshormoner), stimulerer også intracellulær opphopning av kalsium, som igjen bidrar til nevrologiske problemer.

De nevner også, interessant nok, hvorfor MSM har effekt på prestasjon hos idrettsutøvere.

http://www.ncbi.nlm.nih.gov/pubmed/25801485

Abstract

Until now oxygen was thought to be the leading factor of hypoxic conditions. Whereas now it appears that insulin is the key regulator of hypoxic conditions. Insulin seems to regulate the redox state of the organism and to determine the breakpoint of human breath-holding. This new hypoxia-insulin hypotheses might have major clinical relevance. Besides the clinical relevance, this hypothesis could explain, for the first time, why the training of the diaphragm, among other factors, results in an increase in breath-holding performance. Elite freedivers/apnea divers are able to reach static breath-holding times to over 6min. Untrained persons exhibit an unpleasant feeling after more or less a minute. Breath-holding is stopped at the breakpoint. The partial oxygen pressure as well as the carbon dioxide pressure failed to directly influence the breakpoint in earlier studies. The factors that contribute to the breakpoint are still under debate. Under hypoxic conditions the organism needs more glucose, because it changes from the oxygen consuming pentose phosphate (36ATP/glucose molecule) to the anaerobic glycolytic pathway (2ATP/glucose molecule). Hence insulin, as it promotes the absorption of glucose, is set in the center of interest regarding hypoxic conditions. This paper provides an insulin based model that could explain the changes and interactions in human breath-holding. The correlation between hypoxia and reactive oxygen species (ROS) and their influence on the sympathetic nerve system and hypoxia-inducible factor 1 alpha (HIF-1α) is dealt with. It reviews as well the direct interrelation of HIF-1α and insulin. The depression of insulin secretion through the vagus nerve activation via inspiration is discussed. Furthermore the paper describes the action of insulin on the carotid bodies and the diaphragm and therefore a possible role in respiration pattern. Freedivers that go over the breakpoint of breath-holding could exhibit seizures and thus the effect of insulin, blood glucose levels and corticosteroids in hippocampal seizures is highlighted.

It is accepted that under hypoxic condi- tions the brain switches from the oxygen consuming pentose phos- phate to the glycolytic pathway [21]. Furthermore it has been shown that depending on the paradigm used and brain regions during activation under normoxia, the nonoxidative metabolism increases more than the oxidative one [22]. This strengthens the role of glucose as a major fuel for the brain. Insulin has been shown to reduce hippocampal injury after ischemia [23]. Therefore insulin is a potential key regulator in hypoxic conditions when considering these facts.

The effect of ROS on the musculature is a dose dependent influence on the mus- cle force. In low concentration it increases the muscle force, at high levels it decreases it [28,29] (Fig. 1; Arrow 6, 7). Therefore the redox state of the muscle could be a regulation tool of the isometric muscle force [30]. A possible explanation is that increased ROS pro- duction can alter the calcium release from the sarcoplasmic reticu- lum and also the calcium sensitivity of myofilaments [28,30].

It has been shown that antioxidants can prevent muscular fatigue [31]. The ROS-scavenger N-acetylcysteine [32], as a supporter for glu- tathione resynthesis, postpones the muscle fatigue of an in situ prepared diaphragm [31]. These findings are in line with the reports of elite freedivers that antioxidants like vitamin E, C, resveratrol, methylsulfonylmethane, NAC, coenzyme Q10 etc. have a positive effect on their (static) performance.

During inspiration there should normally be no lack of oxygen and therefore no need for extra insulin. But if there were a lack of oxygen, the organism needs an escape mechanism. This could be accomplished by the previously described rise of ROS, and therefore, via HIF1-a, an increase in the insulin level.

In hypoxic conditions, it appears as insulin secretion rises with increased HIF-a levels.

Insulin triggers the carotid bodies, which should result in diaphragmatic movements.

During breath-holding, insulin secretion is decreased through the activated afferent vagus nerve via the pulmonary stretch receptors. As long as the diaphragm can be hold contracted the stretch receptors are triggered and therefore the insulin secretion is diminished. Hence explaining why training of breath-holding, or better the training of the dia- phragm, results in increased breath-holding performances.

So it seems that insulin is more or less a key regulator in hypoxic conditions. It has to be taken into consideration that under hypoxic situations the organism has to switch to anaerobic meta- bolism and therefore is in need of more glucose. Hence insulin is put into the spotlight of interest when it comes to metabolism under hypoxic conditions and a relative maintenance of a survival fitting redox state

Is Objectively Measured Sitting Time Associated with Low Back Pain? A Cross-Sectional Investigation in the NOMAD study

Studie som viser hvordan stillesitting henger sammen med korsryggsmerter hos kontorarbeidere. Jo lenger man sitter stille jo lettere er det å få smerter.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4373888/

Adults generally spend as much as 6–8 hours per day or more than 45–50% of their waking hours in a sitting position [913].

We found a significant positive association between leisure-time sitting and LBP, even after adjusting for various potential individual and work-related confounders. A similar clear association was observed when we analyzed the association between categories (low, moderate, high) of leisure-time sitting and LBP.

Non-specific low back pain: occupational or lifestyle consequences?

Denne nevner at risikofaktorene for korsryggsmerter ikke egentlig er så godt assosiert med arbeid og mekaniske faktorer i f.eks. løfting hos sykepleiere. Det er større risikofaktorer i andre faktorer, som: arbeidsmiljø, livsstil, livskvalitet, m.m.

http://www.ncbi.nlm.nih.gov/pubmed/25821057/?ncbi_mmode=std

Abstract

BACKGROUND:

Nursing occupation was identified as a risk occupation for the development of low back pain (LBP). The aim of our study was to find out how much occupational factors influence the development of LBP in hospital nursing personnel.

PATIENTS AND METHODS:

Non-experimental approach with a cross-sectional survey and statistical analysis. Nine hundred questionnaires were distributed among nursing personnel, 663 were returned and 659 (73.2 %) were considered for the analysis. Univariate and multivariate statistics for LBP risk was calculated by the binary logistic regression. The χ2, influence factor, 95 % confidence interval and P value were calculated. Multivariate binary logistic regression was calculated by the Wald method to omit insignificant variables.

RESULTS:

Not performing exercises represented the highest risk for the development of LBP (OR 2.8, 95 % CI 1.7-4.4; p < 0.001). The second and third ranked risk factors were frequent manual lifting > 10 kg (OR 2.4, 95 % CI 1.5-3.8; p < 0.001) and duration of employment ≥ 19 years (OR 2.4, 95 % CI 1.6-3.7; p < 0.001). The fourth ranked risk factor was better physical condition by frequent recreation and sports, which reduced the risk for the development of LBP (OR 0.4, 95 % CI 0.3-0.7; p = 0.001). Work with the computer ≥ 2 h per day as last significant risk factor also reduced the risk for the development of LBP (OR 0.6, 95 % CI 0.4-0.1; p = 0.049).

CONCLUSION:

Risk factors for LBP established in our study (exercises, duration of employment, frequent manual lifting, recreation and sports and work with the computer) are not specifically linked to the working environment of the nursing personnel. Rather than focusing on mechanical causes and direct workload in the development of non-specific LBP, the complex approach to LBP including genetics, psychosocial environment, lifestyle and quality of life is coming more to the fore.

Six Persistent Research Misconceptions

Denne beskriver misforståelser som gjøre i vitenskap, både av forskere og i lærebokene. Bl.a. hvordan man legger for mye vekt på enkelt elementer i den vitenskapelige metode. Og hvordan mange avfeier forskningsresultater alt for fort ved å si at det er «statistisk usignifikant».

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4061362/

It is easy to declare that a result is not statistically significant, falsely implying that there is no indication of an association, rather than to consider quantitatively the range of associations that the data actually support. These misconceptions involve taking the low road, but when that road is crowded with others taking the same path, there may be little reason to question the route. Indeed, these misconceptions are often perpetuated in journals, classrooms and textbooks.