Stikkordarkiv: Smerte

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Smertens nevrobiologi

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Per Brodal, en av norges fremst nevrologer, skrev i 2005 en artikkel i Tidsskriftet om smertens nevrobiologi hvor han nevner mye av den nye forståelsen for smerte og referer til Melzack og Wall forskning.

http://tidsskriftet.no/article/1252875#reference-4

En annen innfallsvinkel fremhever smerteopplevelsens avhengighet av sammenhengen den opptrer i, av tidligere opplevelser og ikke minst av forventninger. Faktisk er smerteopplevelse ofte dårlig korrelert til grad av nociseptoraktivering (4). Smerteopplevelse kan derfor også forstås som en tolking av tilgjengelig informasjon (5).

Et hovedpoeng er at for å forstå smerte må man ta med den store betydningen av kognitive og emosjonelle forhold. Følgende spissformulering av Ramachandran & Blakeslee (5), basert på studier av pasienter med fantomsmerter, peker på betydningen av å søke etter mening bak smerteopplevelsen: «…pain is an opinion on the organism’s state of health rather than a mere reflexive response to an injury».

  • Smertesystemenes normale oppgaver er å beskytte og å gi instruks om hensiktsmessig atferd

  • Smertesystemenes plastisitet gjør dem sårbare for feiltilpasninger som kan medføre spontan smerte og abnorm reaksjon på trivielle stimuli

  • En del smertetilstander kan best forstås som hjernens tolking av kroppens tilstand på basis av ufullstendig og konfliktfylt informasjon

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noen studier om placeboeffekt ved kirurgi

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Randomised Trial Support for Orthopaedic Surgical Procedures

Denne nevner at den samlede bevismengde for ortopediske inngrep viser at operasjoner ikke er bedre enn ikke-operativ behandling. Den nevner at kirurger forholder seg mindre (25%) til evidensbasert medisin enn andre leger (53%). Jeg legger merke til at kun 53% av avgjørelsene legene tar er evidensbaserte, den andre halvdelen av avgjørelser er det altså ikke evidens for.

The level of RCT support for common orthopaedic procedures compares unfavourably with other fields of medicine.

Empirical research has shown that healthcare decisions on medical wards are more likely to be based on randomised trial evidence (53%) [5] than those on surgical wards (24% to 26%) [6]–[8].

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4057075/

Randomised Trial Support for Orthopaedic Surgical Procedures

Denne nevner at i 50% av de undersøkte kirurgiske inngrepene er det ikke evidens for at det er bedre enn placebo.

Placebo controlled trial is a powerful, feasible way of showing the efficacy of surgical procedures. The risks of adverse effects associated with the placebo are small. In half of the studies, the results provide evidence against continued use of the investigated surgical procedures. Without well designed placebo controlled trials of surgery, ineffective treatment may continue unchallenged.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4029190/

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FORMIs Gule Flagg liste

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Mange behandlere overser med vilje kostholdets forhold til smertetilstander. Av en eller annen grunn opplever de at mat spiller en svært lite rolle. Men dette er et blindfelt i deres persepsjonsevne som gjør at de ikke forholder seg til realitetene og snyter pasientene for mulig symptombedring.

Selv i de Nasjonale retningslinjene for korsryggsmerter sin liste over Gule Flagg (faktorer som bidrar til kroniske smertetilstander) står «problemer med mage» oppført. Dette i seg selv burde være nok til at ALLE behandlere som er i kontakt med smertepasienter setter seg inn i kostholdets betydning.

Gule flagg

Risikofaktorer (hovedsakelig psykososiale) for å utvikle mer langvarige ryggplager

• Arbeidsrelaterte problemer/sykmelding (bør tidsbegrenses)

• Emosjonelle problemer (f.eks depresjon og angst)

• Tilleggsymptomer i form av generaliserte smerter, hodepine, tretthet, svimmelhet og plager fra magen

• Pasienter med omfattende tidligere ryggplager og med nerverotaffeksjon

• Pessimistiske/negative holdninger/overbevisninger i forhold til smertene, f.eks uttalt engstelse for visse bevegelser og for å være i arbeid, og liten grad av forventning om å bli bra/komme tilbake i arbeid

Klikk for å få tilgang til Kortversjon.pdf

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Sleep in Elite Athletes and Nutritional Interventions to Enhance Sleep

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Beskriver forskjellige måter søvn påvirker atleter, og hvordan søv påvirkes av mat. Nevner at høykarbo mat må inntaes minimum 1t før leggetid.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008810/

The same research group also increased the sleep time of swimmers from their usual sleep amount to 10 h per night for 6–7 weeks. Following this period, 15 m sprint, reaction time, turn time, and mood all improved [30].

Waterhouse et al. [31] investigated the effects of a lunchtime nap on sprint performance following partial sleep deprivation (4 h of sleep). Following a 30-min nap, 20 m sprint performance was increased, alertness was increased, and sleepiness was decreased when compared with the no-nap trial. In terms of cognitive performance, sleep supplementation in the form of napping has been shown to have a positive influence on cognitive tasks following a night of sleep deprivation (2 h) [32]. Naps can markedly reduce sleepiness and can be beneficial when learning skills, strategy or tactics [32]. Napping may also be beneficial for athletes who have to wake early routinely for training or competition and those who are experiencing sleep deprivation [32].

Pain Perception

It is well accepted that individuals with chronic pain frequently report disturbed sleep (changes in continuity of sleep as well as sleep architecture). However, there is also recent evidence suggesting that sleep deprivation may cause or modulate acute and chronic pain [36]. Sleep deprivation may thus enhance or cause pain, and pain may disturb sleep by inducing arousals during sleep. A cycle may then eventuate, starting with either pain or sleep deprivation, with these two issues maintaining or augmenting each other [36].

Athletes may experience pain as a result of training, competition and/or injury. Evidence, although minimal at this stage, suggests that athletes may also have lower sleep quality and quantity than the general population [16]. Therefore, appropriate pain management as well as adequate sleep is likely to be very important for athletes from both a pain and sleep perspective.

A small number of studies have investigated the effects of carbohydrate ingestion on indices of sleep quality and quantity. Porter and Horne [52] provided six male subjects with a high-carbohydrate meal (130 g), a low-carbohydrate meal (47 g), or a meal containing no carbohydrate, 45 min before bedtime. The high-carbohydrate meal resulted in increased REM sleep, decreased light sleep, and wakefulness [52].

Practical Applications

In the first instance, athletes should focus on utilizing good sleep hygiene to maximize sleep quality and quantity. While research is minimal and somewhat inconclusive, several practical recommendations may be suggested:

  • High GI foods such as white rice, pasta, bread, and potatoes may promote sleep; however, they should be consumed more than 1 h before bedtime.
  • Diets high in carbohydrate may result in shorter sleep latencies.
  • Diets high in protein may result in improved sleep quality.
  • Diets high in fat may negatively influence total sleep time.
  • When total caloric intake is decreased, sleep quality may be disturbed.
  • Small doses of tryptophan (1 g) may improve both sleep latency and sleep quality. This can be achieved by consuming approximately 300 g of turkey or approximately 200 g of pumpkin seeds.
  • The hormone melatonin and foods that have a high melatonin concentration may decrease sleep onset time.
  • Subjective sleep quality may be improved with the ingestion of the herb valerian; however, as with all supplements, athletes should be aware of potential contaminants as well as the inadvertent risk of a positive drug test.
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David Butler forklarer «smudging»

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David Butler er en av våre største inspirasjonskilder når det gjelder å forstå hvordan smerte fungerer, og hva vi kan gjøre med det.

Her forklarer han hvordan hjernens opplevelse av kroppen endres ved langvarig smerte. Han kaller det «smudging». Hjernens kart over kroppen blir utydelig. Han forklarer også hvordan dette kan trenes opp igjen.

Hjernen er ekstremt plastisk, foranderlig og tilpasningsdyktig. På Verkstedet gjør vi alt vi kan for å gi hjernen og nervesystemet bedre vilkår å tilpasse seg til: The Founder, ernæring, pust og god behandling.

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Elevated Inflammatory Markers in Response to Prolonged Sleep Restriction Are Associated With Increased Pain Experience in Healthy Volunteers

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Denne nevner at 10 dager med redusert søvn (4 timer) øker betennelsesfaktorer i kroppen. 4 timers søvn er svært lite og de fleste sover nok mer enn dette, men studien nevner at 25% reduksjon (6 timer) også gir en økning i betennelsesfaktorer, dog ikke like kraftig.

Den nederste grafen viser hvordan ubehag i kroppen henger sammen med økning i betennelsesfaktorer.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1978405/

Conclusion:

Insufficient sleep quantity may facilitate and/or exacerbate pain through elevations of IL-6. In disorders where sleep disturbances are common, insufficient sleep quantity itself may establish and maintain its co-occurrence with pain and increased inflammation.

Acute sleep loss of up to 3 nights15,17,18 as well as more commonly experienced forms of sleep loss, i.e., sleep reduced by 25%-50% across consecutive days,18,19 have been shown to induce an increase of interleukin-6 (IL-6) and C-reactive Protein (CRP) levels. In addition, increased levels of IL-6 have been found in patients suffering from primary insomnia.20,21

Pain is a hallmark of inflammatory processes. Prostaglandins, in particular PGE2, are classical pain mediators, but in the last decade a variety of novel pain modulators have been identified. For example, proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) have been found to be potent pain-inducing and pain-facilitating agents, able to sensitize primary sensory neurons.26

Ten days of sleep restriction to 50% of the habitual time led to an IL-6 increase of 1.16 pg/mL in the current study. Sleep restriction to approximately 25% of usual sleep time over one week has been found to lead to a slightly smaller IL-6 increase of 0.75 pg/mL compared to the present result.19 This may suggest a dose-response relationship between chronicity/severity of sleep restriction and elevation of IL-6 levels, and warrants further investigation.

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Pain Sensitivity and Recovery From Mild Chronic Sleep Loss

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Denne viser at økt søvnmengde reduserer smerte. Ved å øke antall timer søvn fra (under) 8 timer til 10 timer ble deltakerene mindre sensitive for smertestimuli. Den nevner også at vi sover mindre nå enn vi gjorde på 60-tallet. Nå er vi nede i 6 timer eller mindre, mens på 60-tallet sov vi 8 timer eller mindre. Den nevner også vi vi får 24%-31% mindre smertetåleranse om vi får 50% dårligere søvn 1 enkelt natt.

Studien beskriver at 4 dager med 10 timers søvn reduserer smertesensitivitet med 25%.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3490359/

Abstract

Study Objectives:

To determine whether an extended bedtime in sleepy and otherwise healthy volunteers would increase alertness and thereby also reduce pain sensitivity.

Setting:

Outpatient with sleep laboratory assessments.

Participants and Interventions:

Healthy volunteers (n = 18), defined as having an average daily sleep latency on the Multiple Sleep Latency Test (MSLT) < 8 min, were randomized to 4 nights of extended bedtime (10 hr) (EXT) or 4 nights of their diary-reported habitual bedtimes (HAB). On day 1 and day 4 they received a standard MSLT (10:00, 12:00, 14:00, and 16:00 hr) and finger withdrawal latency pain testing to a radiant heat stimulus (10:30 and 14:30 hr).

Results:

During the four experimental nights the EXT group slept 1.8 hr per night more than the HAB group and average daily sleep latency on the MSLT increased in the EXT group, but not the HAB group. Similarly, finger withdrawal latency was increased (pain sensitivity was reduced) in the EXT group but not the HAB group. The nightly increase in sleep time during the four experimental nights was correlated with the improvement in MSLT, which in turn was correlated with reduced pain sensitivity.

Conclusions:

These are the first data to show that an extended bedtime in mildly sleepy healthy adults, which resulted in increased sleep time and reduced sleepiness, reduces pain sensitivity.

In the 1960s sleep duration was estimated to be approximately 8 hr per 24-hr period, whereas by 2005 it was reported that sleep duration was 7 hr or less.3 A national survey reported that 21% of the population obtains 6 hr or less of sleep per 24-hr period.4

Partial deprivation, the reduction of bedtime by 50% for one night, reduced finger withdrawal latency (increased pain sensitivity) to a radiant heat stimulus by 24%.7

In the EXT group of the current study finger withdrawal latency was increased by 25%, which reflects a reduction in pain sensitivity.

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Exploring the associations between sleep problems and chronic musculoskeletal pain in adolescents: A prospective cohort study

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Denne nevner at søvnproblemer i ungdommen gir utgangspunkt for smerteproblemer senere i livet. Det er vanlig å tro at smerteproblemer gir søvnproblemer, men denne viser at søvnproblemer ofte kommer før smerteproblemer.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4197758/

Abstract

BACKGROUND:

The prevalence of musculoskeletal chronic pain in adolescents is estimated to be approximately 4% to 40%. The development of musculoskeletal pain during teenage years could have a marked impact on physical, psychological and social well-being.

OBJECTIVE:

To examine whether sleep problems during adolescence are associated with musculoskeletal pain, particularly chronic regional pain and chronic widespread pain.

METHODS:

Using data from the Avon Longitudinal Study of Children, the relationship between sleep problems at 15 years of age and the presence of chronic regional and widespread pain at 17 years of age was explored. Pain data were not available at 15 years of age. A total of 2493 participants with complete data were identified. Relationships among sleep problems and musculoskeletal pain were examined using logistic regression. ORs were calculated after adjusting for sex, ethnicity, socioeconomic position and depression (15 years of age).

RESULTS:

Sleep disturbance (usually wakes up more than two or three times), difficulties with hypersomnolence and poor subjective sleep perception were associated with the presence of both musculoskeletal regional and widespread pain. Finally, using ordered logistic regression, poor subjective sleep perception was also found to be associated with greater pain severity in participants with chronic musculoskeletal regional and widespread pain.

DISCUSSION:

The results of the present study suggest an association between sleep problems during adolescence and the presence of musculoskeletal pain at a later stage. These findings are consistent with adult literature suggesting a link between sleep problems and musculoskeletal pain. Given these associations, sleep problems in adolescence may be an important risk factor for musculoskeletal pain.

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Motor Imagery in People With a History of Back Pain, Current Back Pain, Both, or Neither

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Nevner at for mennesker med ryggsmerte er hjernens opplevelse av kroppen og dens bevegelser dårligere. Hjernens kart over kroppen blir utydelig. Dette kartet er noe av det første vi vil gjenopprette. Det er en viktig del av behandling, og en av de viktigste årsakene til at vi anbefaler daglige øvelser, som f.eks. Foundation trening.

http://www.ncbi.nlm.nih.gov/pubmed/24535054

Introduction:

There is mounting evidence that cortical maps are disrupted in chronic limb pain and that these disruptions may contribute to the problem and be a viable target for treatment. Little is known as to whether this is also the case for the most common and costly chronic pain—back pain.

Objectives:

To investigate the effects of back pain characteristics on the performance of left/right trunk judgment tasks, a method of testing the integrity of cortical maps.

Methods:

A total of 1008 volunteers completed an online left/right trunk judgment task in which they judged whether a model was rotated or laterally flexed to the left or right in a series of images.

Results:

Participants who had back pain at the time of testing were less accurate than pain-free controls (P=0.027), as were participants who were pain free but had a history of back pain (P<0.01). However, these results were driven by an interaction such that those with current back pain and a history of back pain were less accurate (mean [95% CI]=76% [74%-78%]) than all other groups (>84% [83%-85%]).

Discussion:

Trunk motor imagery performance is reduced in people with a history of back pain when they are in a current episode. This is consistent with disruption of cortical proprioceptive representation of the trunk in this group. On the basis of this result, we propose a conceptual model speculating a role of this measure in understanding the development of chronic back pain, a model that can be tested in future studies.

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Neuropathic pain: diagnosis, pathophysiological mechanisms, and treatment

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Denne nevner det aller meste om diagnostisering og behandling av nevropatiske smerter. Her fokuseres på medisiner, men de nevner at en interdisiplinær behandling er viktig.

http://www.thelancet.com/journals/laneur/article/PIIS1474-4422(10)70143-5/fulltext

Neuropathic pain develops as a result of lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Examples of neuropathic pain include painful polyneuropathy, postherpetic neuralgia, trigeminal neuralgia, and post-stroke pain. Clinically, neuropathic pain is characterised by spontaneous ongoing or shooting pain and evoked amplified pain responses after noxious or non-noxious stimuli. Methods such as questionnaires for screening and assessment focus on the presence and quality of neuropathic pain. Basic research is enabling the identification of different pathophysiological mechanisms, and clinical assessment of symptoms and signs can help to determine which mechanisms are involved in specific neuropathic pain disorders. Management of neuropathic pain requires an interdisciplinary approach, centred around pharmacological treatment. A better understanding of neuropathic pain and, in particular, of the translation of pathophysiological mechanisms into sensory signs will lead to a more effective and specific mechanism-based treatment approach.