Dette klippet nevner forskningen til den svenske nevrokirurgen Alfred Breig og viser til at det er hofteleddet som bestemmer det meste i nervesystemets tensjon (strekk). Utoverrotasjon og lett abduksjon gir minst strekk i nervesystemet.
«Tension in the nervous system has the same effect as compression» – Barret Dorko
Omfattende studie om kronisk smerte som kommer med reelle tiltak for å bedre tilstanden hos pasientene. Nevner spesielt en at en holdningsendring må skje hos legene og sykepleierene hvor man inkluderer pasientes subjektive opplevelse. Nevner grunnlaget for dagens medisin og objektifisering av pasienten: «Foucault412 described the paradoxical position of the clinical encounter, in which the doctor aims to diagnose a disease rather than understand the person’s experience: ‘If one wishes to know the illness from which he is suffering, one must subtract the individual, with his [or her] particular qualities’ »
http://www.journalslibrary.nihr.ac.uk/__data/assets/pdf_file/0010/94285/FullReport-hsdr01120.pdf
Conclusion: Our model helps us to understand the experience of people with chronic MSK pain as a constant adversarial struggle. This may distinguish it from other types of pain. This study opens up possibilities for therapies that aim to help a person to move forward alongside pain. Our findings call on us to challenge some of the cultural notions about illness, in particular the expectation of achieving a diagnosis and cure. Cultural expectations are deep-rooted and can deeply affect the experience of pain. We therefore should incorporate cultural categories into our understanding of pain. Not feeling believed can have an impact on a person’s participation in everyday life. The qualitative studies in this meta-ethnography revealed that people with chronic MSK pain still do not feel believed. This has clear implications for clinical practice. Our model suggests that central to the relationship between patient and practitioner is the recognition of the patient as a person whose life has been deeply changed by pain. Listening to a person’s narratives can help us to understand the impact of pain. Our model suggests that feeling valued is not simply an adjunct to the therapy, but central to it. Further conceptual syntheses would help us make qualitative research accessible to a wider relevant audience. Further primary qualitative research focusing on reconciling acceptance with moving forward with pain might help us to further understand the experience of pain. Our study highlights the need for research to explore educational strategies aimed at improving patients’ and clinicians’ experience of care.
As part of a person’s struggle we described the fragmentation of body and self, and suggested that moving forward with pain involves a process of reintegrating the painful body.
Under conditions of health, we perform actions automatically and remain unaware of our body until something goes wrong with it. Health presupposes that we remain unaware of our bodies.396 When in pain, the body emerges as an ‘alien presence’;
it ‘dys-appears’. I no longer am a body but have a body,388 and my body becomes an ‘it’ as opposed to an
I’. Wall399 describes this dualism as epitomised by the expression ‘my foot hurts me’ as if in some way the foot is apart from myself (p. 23). It is because ‘the body seizes our awareness particularly at times of disturbance, [that] it can come to appear “other” and opposed to the self’ (p. 70).388 This fragmentation of ‘mind trapped inside an alien body’ means that our bodies become mistrusted and ‘forgotten as a ground of knowledge’ (p. 86).388 Our concept ‘integrating my painful body’ implies an altered therapeutic relationship with the body in which the dualism of mind and body are broken down.
We do not know why certain patients can accept and redefine their sense of self and others cannot.
It may be related to the degree of disruption to self that is caused by pain. The enmeshment model developed by Pincus and Morley406 proposes that, if a person regards their ideal self as unobtainable in the presence of pain, they are less likely to accept chronic pain. The enmeshment model incorporates self-discrepancy theory,407 which proposes that the extent to which pain disrupts our lives depends on the meaning that it holds for us. In self-discrepancy theory meaning incorporates three constructs: (1) actual self – ‘your representation of the attributes that someone (yourself or another) believes you actually possess’; (2) ideal self – ‘your representation of the attributes that someone (yourself or another) would like you, ideally, to possess’; and (3) ought self – ‘your representation of the attributes that someone (yourself or another) believes you should or ought to possess’ (p. 320–1).407
However, it is ‘pathos’, the feeling of suffering and powerlessness, of ‘life going wrong’, that precedes a person’s visit to the doctor (p. 137).396 Our model suggests that central to the therapeutic relationship is the recognition of ‘pathos’; the patient is a subject rather than an ‘object’ of investigation. This concept is central to models of patient-centred care.413
We described a need for a person in pain to feel that the health-care professional is alongside them with their pain. Affirming a person’s experience and allowing an empathetic interpretation of their story is not an adjunct, but integral to health care.395
Our model also suggests possibilities that might help patients to move forward alongside their pain:
Dette er en veldig viktig artikkel for å forstå diafragmas rolle i både pust og bevegelse, og ifh smertetilstander i ryggraden. Nevner en lovende teknikk for å styrke diafragma og støttemuskulatur hvor man blåser opp en ballong og strammer kjernemuskulaturen. Nevner Zone of Apposition (ZOA) som beskriver diafragmas bevegelsesmuligheter. Ved lav ZOA har diafrgma lite bevegelse. Vi ønsker å øke ZOA. Denne øvelsen er konstruert basert på fysioterapeutisk prinsipper, men i Verkstedet Breathing System har vi øvelser som er gir samme resultater på diafragma, men bygget på lang og erfaringsbasert tradisjon fra tibetansk buddhisme.
Nevner også hvordan mage-pust minker bevegelsen i diafragma.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2971640/
Suboptimal breathing patterns and impairments of posture and trunk stability are often associated with musculoskeletal complaints such as low back pain. A therapeutic exercise that promotes optimal posture (diaphragm and lumbar spine position), and neuromuscular control of the deep abdominals, diaphragm, and pelvic floor (lumbar-pelvic stabilization) is desirable for utilization with patients who demonstrate suboptimal respiration and posture. This clinical suggestion presents a therapeutic exercise called the 90/90 bridge with ball and balloon. This exercise was designed to optimize breathing and enhance both posture and stability in order to improve function and/or decrease pain. Research and theory related to the technique are also discussed.
Many muscles used for postural control/stabilization and for respiration are the same, for example: the diaphragm, transversus abdominis, and muscles comprising the pelvic floor.1–6 Maintaining optimal posture/stability and respiration is important and is even more challenging during exercise. Exercise increases respiratory demand (e.g. running) and limb movements (e.g. arms moving while standing still) increase postural demands for stabilization.3,7
Many factors are potentially involved with suboptimal respiration and suboptimal (faulty) posture and may be associated with musculoskeletal complaints such as low back pain, and/or sacroiliac joint pain.8 (Table 1)
| Suboptimal Respiration and Posture |
| Decreased/suboptimal Zone of Apposition of diaphragm |
| Decreased exercise tolerance |
| Decreased intra-abdominal pressure |
| Shortness of Breath/Dyspnea |
| Decreased respiratory efficiency |
| Decreased expansion of lower rib cage/chest |
| Decreased appositional diaphragm force |
| Decreased length of diaphragm (short) |
| Decreased transdiaphragm pressure |
| Increased use of accessory muscles of respiration |
| Poor neuromuscular control of core muscles |
| Increased lumbar lordosis |
| Increased anterior pelvic tilt |
| Increased hamstring length |
| Increased abdominal length |
| Rib elevation/external rotation |
| Sternum elevation |
| Increased activity of paraspinals |
| Increased lumbar-pelvic instability |
| Low back pain |
| Sacroiliac Joint pain |
| Thoracic Outlet Syndrome |
| Headaches |
| Asthma |
One of the most critical factors, often overlooked by physical therapists, is maintaining an optimal zone of apposition of the diaphragm.3,9–11 The zone of apposition (ZOA) is the area of the diaphragm encompassing the cylindrical portion (the part of the muscle shaped like a dome/umbrella) which corresponds to the portion directly apposed to the inner aspect of the lower rib cage.12 The ZOA is important because it is controlled by the abdominal muscles and directs diaphragmatic tension. When the ZOA is decreased or suboptimal, there are several potential negative consequences. (Table 1) Two examples include:
The incidence of LBP has been documented to be as high as 30% in the athletic population, and in many cases pain may persist for years.15 Low back pain is frequently correlated with faulty posture such as an excessive lumbar lordosis.16–18 Excessive lumbar lordosis may be associated with over lengthened and weak abdominal musculature.18–20 Poor neuromuscular control of core muscles (transversus abdominis, internal oblique, pelvic floor and diaphragm) has been described in individuals with SIJ pain21 and in individuals with lumbar segmental instability, potentially adversely affecting respiration.22
Richardson et al.27 describe coordination of the Transversus abdominis and the diaphragm in respiration during tasks in which stability is maintained by tonic activity of these muscles. During inspiration, the diaphragm contracts concentrically, whereas the transversus abdominis contracts eccentrically. The muscles function in reverse during exhalation with the diaphragm contracting eccentrically while the transversus abdominis contracts concentrically. Hodges et al. noted that during respiratory disease the coordinating function between the transversus abdominis and diaphragm was reduced.6 Thus, it is also possible that faulty posture such as over lengthened abdominals and excessive lordosis could reduce the coordination of the diaphragm and transversus abdominis during respiration and stabilization activities.
O’sullivan et al.21 studied subjects with LBP attributed to the sacroiliac joints and compared them to control subjects without pain. O’sullivan et al. compared respiratory rate and diaphragm and pelvic floor movement using real time ultrasound during a task that required load transfer through the lumbo-pelvic region (the active straight leg raise test). Subjects with pain had an increase in respiratory rate, descent of their pelvic floor and a decrease in diaphragm excursion as compared to the control subjects, who had normal respiratory rates, less pelvic floor descent, and optimal diaphragm excursion. While O’sullivan et al. concluded that an intervention program focused on integrating control of deep abdominal muscles with normal pelvic floor and diaphragm function may be effective in managing patients with LBP,21 they did not describe strategies or exercises to achieve this goal.21
While the role of the Transversus abdominis in lumbar stability is well documented, less well known is the role of the diaphragm in lumbar stability. While the primary function of the diaphragm is respiration, it also plays a role in spinal stability.3,28
The right hemidiaphragm attaches distally to the anterior portions of the first through third lumbar vertebrae (L1-3) and the left hemidiaphragm attaches distally on the first and second lumbar vertebrae (L1-2).29 This section of the diaphragm is referred to as the crura. Of interest is the asymmetrical attachment of the diaphragm with the left hemidiaphragm attaching to L1-2 and the right portion attaching to L1-3.
During the inhalation phase of ventilation, the dome of the diaphragm moves caudally like a piston creating a negative pressure in the thorax that forces air into the lungs. This action is normally accompanied by a rotation of the ribs outward (external rotation) largely in part due to the ZOA.12 (Figure 1) Apposition is a term that means multiple layers adjacent to each other.33 The normal force of pull on the sternal and costal portions of the diaphragm would produce an internal rotation of the ribs. The ZOA creates an external rotation of these ribs primarily because the pressure in the thoracic cavity prevents an inward motion. The crural portion of the diaphragm assists the caudal motion of the dome. It also pulls the anterior lumbar spine upward (cephalad and anterior). Additionally, the abdominal muscles and pelvic floor musculature are less active to allow visceral displacement due to the dome of the diaphragm dropping. With exhalation, this process is reversed. Abdominal muscle activity compresses the viscera in the abdominal cavity, the diaphragm is forced cephalad and the ribs internally rotate. As exhalation becomes forced as during exercise, abdominal activity (rectus abdominus, internal obliques, external obliques, and transversus abdominis) will be increased.34–36
When the ZOA is optimized, the respiratory and postural roles of the diaphragm have maximal efficiency.37 In suboptimal positions (i.e. decreased ZOA), the diaphragm has a decreased ability to draw air into the thorax because of less caudal movement upon contraction and less effective tangential tension of the diaphragm on the ribs and therefore lower transdiaphragmatic pressure.38 This decreased ZOA is accompanied by decreased expansion of the rib cage, postural alterations, and a compensatory increase in abdominal expansion.12 (Figure 2)
One such adaptive breathing strategy would be to relax the abdominal musculature more than necessary on inspiration to allow for thoraco-abdominal expansion. This situation leads to decreased abdominal responsibility while breathing and can contribute to instability. This would reflect more upper chest breathing and less efficient diaphragm activity. If the body maintains this position and breathing strategy for an extended period of time, the diaphragm may adaptively shorten and the lungs may become hyperinflated.37,39,40 Hyperinflation may also contribute to over use of accessory muscles of respiration such as scalenes, sternocleidomastoid (SCM), pectorals, upper trapezius and paraspinals in an attempt to expand the upper rib cage.41–44 Again, without an optimal dome shape/position of the diaphragm or an optimal ZOA the body compensates to get air in with accessory muscles since the more linear/flat/short diaphragm is less efficient for breathing.32
Instructions for Performance of the 90/90 Bridge with Ball and Balloon: 1. Lie on your back with your feet flat on a wall and knees and hips bent at a 90-degree angle. 2. Place a 4-6 inch ball between your knees. 3. Place your right arm above your head and a balloon in your left hand. 4. Inhale through your nose and as you exhale through your mouth, perform a pelvic tilt so that your tailbone is raised slightly off the mat. Keep low back flat on the mat. Do not press your feet into the wall, instead pull down with your heels. 5. You should feel the back of your thighs and inner thighs engage, keeping pressure on the ball. Maintain this position for the remainder of the exercise. 6. Now inhale through your nose and slowly blow out into the balloon. 7. Pause three seconds with your tongue positioned on the roof of your mouth to prevent airflow out of the balloon. 8. Without pinching the neck of the balloon and keeping your tongue on the roof of your mouth, inhale again through your nose. 9. Slowly blow out as you stabilize the balloon with your left hand. 10. Do not strain your neck or cheeks as you blow. 11. After the fourth breath in, pinch the balloon neck and remove it from your mouth. Let the air out of the balloon.12. Relax and repeat the sequence 4 more times. Copyright © Postural Restoration Institute™ 2009, used with permission
The patient/athlete is asked to hold the balloon with one hand and inhale through his/her nose with the tongue on the roof of the mouth (normal rest position) and then exhale through his/her mouth into the balloon. The inhalation, to about 75% of maximum, is typically 3-4 seconds in duration, and the complete exhalation is usually 5-8 seconds long followed by a 2-3 second pause. This slowed breathing is thought to further relax the neuromuscular system/parasympathetic nervous system and generally decrease resting muscle tone. Ideally the patient/athlete will be able to inhale again without pinching off the balloon with their teeth, lips, or fingertips. This requires maintenance of intra-abdominal pressure to allow inhalation through the nose without the air coming back out of the balloon and into the mouth.
When the exercise is performed by the patient/athlete with hamstring and gluteus maximus (glut max) activation (hip extensors) the pelvis moves into a relative posterior pelvic tilt and the ribs into relative depression and internal rotation. This pelvic and rib position helps to optimize abdominal length (decreases) and diaphragm length/ZOA (increases).
Clinical experience with the BBE includes utilization of the exercise for both female and male patients (more females than males), ages 5-89 with a wide variety of diagnoses including: low back pain, trochanteric bursitis, SIJ pain, asthma, COPD, acetabular labral tear, anterior knee pain, thoracic outlet syndrome (TOS) and sciatica.
En studie som gir en tydelig beskrivelse av hvor mye mindfulness demper smerte. De fant ingen korrelasjon mellom pustefrekvens og smertereduksjon, men det kan være flere faktorer som spiller inn der. I denne studien gjorde de f.eks. kun 20 min meditasjon i 4 dager, med mennesker som ikke har meditert først. De andre studiene inkluderer mennesker som har meditert lenge. I tillegg kan man tydelig se at etter 4 dager med meditasjon så blir pustefrekvensen lavere når man blir påført vond varme, noe som tyder på at de begynner å bruke pusten som smertereduksjon. Det var motsatt før de hadde fått instruksjon i meditasjon.
http://www.jneurosci.org/content/31/14/5540.full
After 4 d of mindfulness meditation training, meditating in the presence of noxious stimulation significantly reduced pain unpleasantness by 57% and pain intensity ratings by 40% when compared to rest.
Meditation-induced reductions in pain intensity ratings were associated with increased activity in the anterior cingulate cortex and anterior insula, areas involved in the cognitive regulation of nociceptive processing. Reductions in pain unpleasantness ratings were associated with orbitofrontal cortex activation, an area implicated in reframing the contextual evaluation of sensory events. Moreover, reductions in pain unpleasantness also were associated with thalamic deactivation, which may reflect a limbic gating mechanism involved in modifying interactions between afferent input and executive-order brain areas. Together, these data indicate that meditation engages multiple brain mechanisms that alter the construction of the subjectively available pain experience from afferent information.
Mindfulness-based mental training was performed in four separate, 20 min sessions conducted by a facilitator with >10 years of experience leading similar meditation regimens. Subjects had no previous meditative experience and were informed that such training was secular and taught as the cognitive practice of Shamatha or mindfulness meditation. Each training session was held with one to three participants.
On mindfulness meditation training day 1, subjects were encouraged to sit with a straight posture, eyes closed, and to focus on the changing sensations of the breath occurring at the tips of their nostrils. Instructions emphasized acknowledging discursive thoughts and feelings and to return their attention back to the breath sensation without judgment or emotional reaction whenever such discursive events occurred. On training day 2, participants continued to focus on breath-related nostril sensations and were instructed to “follow the breath,” by mentally noting the rise and fall of the chest and abdomen. The last 10 min were held in silence so subjects could develop their meditative practice. On training day 3, the same basic principles of the previous sessions were reiterated. However, an audio recording of MRI scanner sounds was introduced during the last 10 min of meditation to familiarize subjects with the sounds of the scanner. On the final training session (day 4), subjects received minimal meditation instruction but were required to lie in the supine position and meditate with the audio recording of the MRI sounds to simulate the scanner environment. Contrary to traditional mindfulness-based training programs, subjects were not required to practice outside of training.
Subjects also completed the Freiburg Mindfulness Inventory short-form (FMI), a 14-item assessment that measures levels of mindfulness, before psychophysical pain training and after MRI session 2. The FMI is a psychometrically validated instrument with high internal consistency (Cronbach α = 0.86) (Walach et al., 2006). Statements such as “I am open to the experience of the present moment” are rated on a five-point scale from 1 (rarely) to 5 (always). Higher scores indicate more skill with the mindfulness technique.
Decreases in respiration rate have been reported previously to predict reductions in pain ratings (Grant and Rainville, 2009; Zautra et al., 2010). In the present data (MRI session 2; n = 14), no significant relationship between the decreased respiration rates and pain intensity (p = 0.22, r = −0.35), pain unpleasantness (p = 0.41, r = −0.24), or FMI ratings (p = 0.42, r = 0.24) was found.
| CBF | Respiration rate | Heart rate | |
|---|---|---|---|
| Session 1 | |||
| Rest: neutral | 74.12 (3.01) | 19.97 (1.29) | 72.53 (2.33) |
| Rest: heat | 71.51 (2.93) | 20.45 (1.11) | 74.79 (2.39) |
| ATB: neutral | 70.69 (3.56) | 17.05 (1.00) | 70.46 (1.79) |
| ATB: heat | 67.90 (3.08) | 19.32 (1.33) | 74.07 (2.19) |
| Session 2 | |||
| Rest: neutral | 68.57 (3.17) | 16.72 (0.82) | 74.82 (3.08) |
| Rest: heat | 66.82 (2.59) | 17.12 (0.93) | 77.32 (2.95) |
| Meditation: neutral | 65.09 (3.59) | 11.55 (0.74) | 73.62 (2.77) |
| Meditation: heat | 65.47 (3.86) | 9.47 (0.67)a | 75.38 (2.70) |
In the present investigation, meditation reduced all subjects’ pain intensity and unpleasantness ratings with decreases ranging from 11 to 70% and from 20 to 93%, respectively.
Meditation likely modulates pain through several mechanisms. First, brain areas not directly related to meditation exhibited altered responses to noxious thermal stimuli. Notably, meditation significantly reduced pain-related afferent processing in SI (Fig. 5), a region long associated with sensory-discriminative processing of nociceptive information (Coghill et al., 1999). Executive-level brain regions (ACC, AI, OFC) are thought to influence SI activity via anatomical pathways traversing the SII, insular, and posterior parietal cortex (Mufson and Mesulam, 1982; Friedman et al., 1986;Vogt and Pandya, 1987). However, because meditation-induced changes in SI were not specifically correlated with reductions in either pain intensity or unpleasantness, this remote tuning may take place at a processing level before the differentiation of nociceptive information into subjective sensory experience.
Second, the magnitude of decreased pain intensity ratings was associated with ACC and right AI activation (Fig. 6). Activation in the mid-cingulate and AI overlapped between meditation and pain, indicating a likely substrate for pain modulation. Converging lines of evidence suggest that these regions play a major role in the evaluation of pain intensity and fine-tuning afferent processing in a context-relevant manner (Koyama et al., 2005; Oshiro et al., 2009;Starr et al., 2009). Such roles are consistent with the aspect of mindfulness meditation that involves reducing appraisals that normally impart significance to salient sensory events.
Third, OFC activation was associated with decreases in pain unpleasantness ratings (Fig. 6). The OFC has been implicated in regulating affective responses by manipulating the contextual evaluation of sensory events (Rolls and Grabenhorst, 2008) and processing reward value in the cognitive modulation of pain (Petrovic and Ingvar, 2002). Meditation directly improves mood (Zeidan et al., 2010a), and positive mood induction reduces pain ratings (Villemure and Bushnell, 2009). Therefore, meditation-related OFC activation may reflect altered executive-level reappraisals to consciously process reward and hedonic experiences (e.g., immediate pain relief, positive mood) (O’Doherty et al., 2001; Baliki et al., 2010; Peters and Büchel, 2010).
Studie som nevner at Mindfulness øker alpha-bølger i hjernen, som bidrar til reduksjon i smerte.
http://www.frontiersin.org/Journal/10.3389/fnhum.2013.00012/full
Using a common set of mindfulness exercises, mindfulness based stress reduction (MBSR) and mindfulness based cognitive therapy (MBCT) have been shown to reduce distress in chronic pain and decrease risk of depression relapse. These standardized mindfulness (ST-Mindfulness) practices predominantly require attending to breath and body sensations.
Based on multiple randomized clinical trials, there is good evidence for the efficacy of these ST-Mindfulness programs for preventing mood disorders in people at high risk of depression (Teasdale et al., 2000a,b; Ma and Teasdale, 2004; Segal et al., 2010; Fjorback et al., 2011; Piet and Hougaard, 2011), improving mood and quality of life in chronic pain conditions such as fibromyalgia (Grossman et al., 2007; Sephton et al., 2007; Schmidt et al., 2011) and low-back pain (Morone et al., 2008a,b), in chronic functional disorders such as IBS (Gaylord et al., 2011) and in challenging medical illnesses, including multiple sclerosis (Grossman et al., 2010) and cancer (Speca et al., 2000). ST-Mindfulness has also been shown to decrease stress in healthy people undergoing difficult life situations (Cohen-Katz et al., 2005), such as caring for a loved-one with Alzheimer’s disease (Epstein-Lubow et al., 2006).
Numerous behavioral and neural mechanisms have been proposed to explain these positive outcomes. Proposed mechanisms include changes in neural networks underlying emotion regulation (Holzel et al., 2008), illustrated by findings showing decreased amygdala response after ST-Mindfulness in social anxiety patients exposed to socially threatening stimuli (Goldin and Gross, 2010). Other neural mechanisms highlighted in recent reviews include changes in self-processing (Vago and Silbersweig, 2012) based on multiple studies including a report showing decreases in activation in midline cortical areas used in self-related processing in ST-Mindfulness trained subjects (Farb et al., 2007).
In the first 2 weeks of the 8-week ST-Mindfulness sequence, all formal practice is devoted to a meditative body scan practice of “moving a focused spotlight of attention from one part of the body to another.” Through this exercise, practitioners are said to learn to feel (1) how to control the attentional spotlight even when focusing on painful, aversive sensations (2) how even familiar body sensations change and fluctuate from moment to moment.
In the last 5–6 weeks of class, participants continue to use embodied practices, especially sitting meditation focused on sensations of breathing. These embodied practices are said to teach practitioners (1) how to directlyfeel when the mind has wandered from its sensory focus (2) how to use an intimate familiarity with the fluctuations of sensations of breathing (such as the up and down flow of the breath) as a template for regarding the arising and passing of distressing, aversive thoughts as “mental events” rather than as “facts or central parts of their identity.”
Specifically, we propose that body-focused attentional practice in ST-Mindfulness enhances localized attentional control over the 7–14 Hz alpha rhythm that is thought to play a key role in regulating sensory input to sensory neocortex and in enhancing signal-to-noise properties across the neocortex. Beginning with the enhanced modulation of localized alpha rhythms trained in localized somatic attention practices such as the body-scan, and then proceeding through the 8-week sequence to learn broader modulation of entire sensory modalities (e.g., “whole body attention”) practitioners train in filtering and prioritizing the flow of information through the brain.
In chronic pain situations, nearly all studies of ST-Mindfulness show relief of pain-related distress and increased mood.
Studie på Mindfulness mot kroniske muskelsmerter som sammenlignet effekten av muskelterapi (inkl. bindevev og nevromuskulær behandling – konsepter vi behandler etter på Verkstedet). Muskelterapi var bedre enn Mindfulness mot smerte, men Mindfuness var bedre for psyken på lang sikt. Selv 1 måned etter 8-ukers programmet. Meditasjonsprogrammet vi har på Verkstedet er Verkstedet Breathing System, som gjennom pusten skaper meditative opplevelser og reduksjon av smerte.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1490272/
It is feasible to study MBSR and massage in patients with chronic musculoskeletal pain. Mindfulness-based stress reduction may be more effective and longer-lasting for mood improvement while massage may be more effective for reducing pain.
Mindfulness-based stress reduction is a mind-body intervention described by Kabat-Zinn.18 The participants met weekly for eight 2½ hour sessions. Meditation and yoga techniques were practiced to foster mindfulness (present moment, nonjudgmental awareness). Audiotaped meditation exercises were assigned as daily home practice. Participants were encouraged to use these skills in moments of stress and/or pain.
One-hour massage sessions were given once per week for 8 weeks by 3 licensed massage therapists. Massage techniques were at the discretion of the therapists and included Swedish, deep-tissue, neuromuscular, and pressure-point techniques. We specifically excluded music, scented oils, and energy techniques such as Reiki or therapeutic touch.
En metaanalyse av studier på meditasjonsprogrammer. Konkluderer med at effekten er såpass stor og viktig at leger bør prate med sine pasienter om meditasjon.
http://archinte.jamanetwork.com/article.aspx?articleid=1809754
Mindfulness meditation programs had moderate evidence of improved anxiety (effect size, 0.38 [95% CI, 0.12-0.64] at 8 weeks and 0.22 [0.02-0.43] at 3-6 months), depression (0.30 [0.00-0.59] at 8 weeks and 0.23 [0.05-0.42] at 3-6 months), and pain (0.33 [0.03- 0.62]) and low evidence of improved stress/distress and mental health–related quality of life.
Clinicians should be aware that meditation programs can result in small to moderate reductions of multiple negative dimensions of psychological stress. Thus, clinicians should be prepared to talk with their patients about the role that a meditation program could have in addressing psychological stress.
Reviews to date report a small to moderate effect of mindfulness and mantra meditation techniques in reducing emotional symptoms (eg, anxiety, depression, and stress) and improving physical symptoms (eg, pain).7– 26
Among the 9 RCTs43,44,47,54,55,63,64,73,74 evaluating the effect on pain, we found moderate evidence that mindfulness-based stress reduction reduces pain severity to a small degree when compared with a nonspecific active control, yielding an ES of 0.33 from the meta-analysis. This effect is variable across painful conditions and is based on the results of 4 trials, of which 2 were conducted in patients with musculoskeletal pain,55,64 1 trial in patients with irritable bowel syndrome,43 and 1 trial in a population without pain.44 Visceral pain had a large and statistically significant relative 30% improvement in pain severity, whereas musculoskeletal pain showed 5% to 8% improvements that were considered nonsignificant.
Magnesium gjør at nervesystemet blir mindre sensitivt i studie på rotter med nevropati. Dosen er beregnet til å være ca 147 mg pr dag (24t), som er veldig mye relativt til kroppsvekten på en mus på 10-20g. Om vi regner det om til menneskevekt blir det megadoser.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002451/
Neuropathic pain is a common diabetic complication affecting 8–16% of diabetic patients. It is characterized by aberrant symptoms of spontaneous and stimulus-evoked pain including hyperalgesia and allodynia. Magnesium (Mg) deficiency has been proposed as a factor in the pathogenesis of diabetes-related complications, including neuropathy. In the central nervous system, Mg is also a voltage-dependant blocker of the N-methyl-d-aspartate receptor channels involved in abnormal processing of sensory information. We hypothesized that Mg deficiency might contribute to the development of neuropathic pain and the worsening of clinical and biological signs of diabetes and consequently, that Mg administration could prevent or improve its complications. We examined the effects of oral Mg supplementation (296 mg l−1 in drinking water for 3 weeks) on the development of neuropathic pain and on biological and clinical parameters of diabetes in streptozocin (STZ)-induced diabetic rats. STZ administration induced typical symptoms of type 1 diabetes. The diabetic rats also displayed mechanical hypersensitivity and tactile and thermal allodynia. The level of phosphorylated NMDA receptor NR1 subunit (pNR1) was higher in the spinal dorsal horn of diabetic hyperalgesic/allodynic rats. Magnesium supplementation failed to reduce hyperglycaemia, polyphagia and hypermagnesiuria, or to restore intracellular Mg levels and body growth, but increased insulinaemia and reduced polydipsia. Moreover, it abolished thermal and tactile allodynia, delayed the development of mechanical hypersensitivity, and prevented the increase in spinal cord dorsal horn pNR1. Thus, neuropathic pain symptoms can be attenuated by targeting the Mg-mediated blockade of NMDA receptors, offering new therapeutic opportunities for the management of chronic neuropathic pain.
Diabetes is also the most common pathological state in which secondary magnesium (Mg) deficiency occurs. Indeed, Mg deficiency has been described in 25–30% and 13.5–47.7% of type 1 and type 2 diabetic patients, respectively (Garland, 1992; Tossielo, 1996; Corsonelloet al. 2000; Engelen et al. 2000; Rodriguez-Moran & Guerrero-Romero, 2003; Pham et al.2007) and its incidence is correlated to diabetes complications (De Leeuw, 2001). Mg is an ATPase allosteric effector involved in inositol transport (Grafton et al. 1992) and the impaired Na+/K+-ATPase activity in peripheral nerves of diabetic animals (Garland, 1992) plays a role in the pathophysiology of diabetic neuropathy (Li et al. 2005).
In the central nervous system, Mg has voltage-dependent blocking properties that play an important role in pain processing at the N-methyl-d-aspartate (NMDA) receptor channel complex (Mayer et al. 1984; Xiao & Bennett, 1994; Begon et al. 2000). In vitro, this blockade operates at extracellular Mg concentrations of less than 1 mm (Mayer et al. 1984), i.e. within the ranges found in human and animal cerebrospinal fluid and plasma (Morris, 1992). The excess release of glutamate from central nociceptor terminals due to nerve damage releases Mg blockade and activates NMDA receptors known to trigger painful sensations (hyperalgesia, allodynia) and alter the sensitivity of postsynaptic cells, resulting in central sensitization (Bennett, 2000). This central sensitization involving the NMDA receptor can be induced in rats in vivo by Mg depletion (Alloui et al. 2003). Several studies suggest that phosphorylation of the NMDA receptor NR1 subunit is correlated to the presence of signs of neuropathy and to persistent pain following nerve injury (Gao et al.2005; Ultenius et al. 2006; Gao et al. 2007; Roh et al. 2008).
One week after STZ or distilled water injection, the animals were assigned to the following three experimental groups:
Water intake was 10-fold and sixfold higher in non-supplemented and MgSO4-supplemented STZ-D rats, respectively, compared with non-diabetic rats. Water intake was significantly lower in MgSO4-supplemented STZ-D rats than non-supplemented STZ-D rats (Table 1). Consequently, urine excretion was 24-fold higher in non-supplemented STZ-D rats than non-diabetic rats. The MgSO4-supplemented STZ-D rats also developed polyuria corresponding to a 15-fold increase in urine excretion compared with non-diabetic rats, but which was nevertheless lower than the increase in non-supplemented STZ-D rats (Table 1). Polyuria in STZ-D rats was significantly correlated to water intake (P < 0.001).
| Parameter | Non-diabetic | Non-suppl. STZ-D | MgSO4-suppl. STZ-D |
|---|---|---|---|
| Water intake (ml (24 h)−1) | 35.22 ± 2.36 | 376.6 ± 32.87*** | 214.4 ± 30.87***,### |
| Urine excretion (ml (24 h)−1) | 12.45 ± 1.51 | 300.1 ± 24.16*** | 184.4 ± 25.23***,## |
| Food intake (g (24 h)−1) | 30.7 ± 1.83 | 54.66 ± 3.67** | 42.06 ± 6.21 |
| Total Mg intake (mg (24 h)−1) | 61.40 ± 3.66 | 109.32 ± 7.34*** | 147.58 ± 1.58***,### |
Figure 4: Time course of mechanical sensitivity measured by paw pressure-induced vocalization threshold (VT) variations in non-diabetic (Non-D), non-supplemented STZ-diabetic (Non-suppl. STZ-D) and MgSO4-supplemented (MgSO4-suppl. STZ-D) rats
| Parameter | Non-diabetic | Non-suppl. STZ-D | MgSO4-suppl. STZ-D |
|---|---|---|---|
| Tactile hypersensitivity | |||
| Week 2 | 0/10 | 3/10 | 0/10# |
| Week 4 | 0/10 | 6/10* | 0/10# |
| Thermal hypersensitivity | |||
| Week 2 | 0/10 | 6/10* | 0/10# |
| Week 4 | 0/10 | 6/10* | 0/10# |
This study clearly showed that Mg supplementation prevents tactile and thermal allodynia and attenuates and delays mechanical hyperalgesia in STZ-D rats. This effect was mediated, at least in part, by the prevention of NMDA receptor NR1 subunit phosphorylation in STZ-D rats. However, the study also showed that Mg supplementation did not improve most of the biological and clinical signs of diabetes despite restoration of normal insulin secretion.
Omfattende gjennomgang om hvordan nevrogene betennelser fungerer fysiologisk. Nevner at betennelser ikke er problemet, men en funksjon kroppen benytter seg av for å håndtere problemer som giftstoffer og metabolsk problemer. Derfor nytter det ikke å dempe betennelsen. Man MÅ fjerne årsaken til betennelsen…
http://www.ncbi.nlm.nih.gov/pubmed/24281245
http://www.nature.com/nrn/journal/vaop/ncurrent/full/nrn3617.html
The CNS is endowed with an elaborated response repertoire termed ‘neuroinflammation’, which enables it to cope with pathogens, toxins, traumata and degeneration. On the basis of recent publications, we deduce that orchestrated actions of immune cells, vascular cells and neurons that constitute neuroinflammation are not only provoked by pathological conditions but can also be induced by increased neuronal activity. We suggest that the technical term ‘neurogenic neuroinflammation’ should be used for inflammatory reactions in the CNS in response to neuronal activity. We believe that neurogenic neuro-inflammation maintains homeostasis to enable the CNS to cope with enhanced metabolic demands and increases the computational power and plasticity of CNS neuronal networks. However, neurogenic neuroinflammation may also become maladaptive and aggravate the outcomes of pain, stress and epilepsy.
Nevner at akupunktur er den beste behandling mot uspesifikke ryggsmerter, bedre enn feks. kiropraktisk manipulering.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2223333/
Numerous randomized trials have been published investigating the effectiveness of treatments for non-specific low-back pain (LBP) either by trials comparing interventions with a no-treatment group or comparing different interventions. In trials comparing two interventions, often no differences are found and it raises questions about the basic benefit of each treatment. To estimate the effect sizes of treatments for non-specific LBP compared to no-treatment comparison groups, we searched for randomized controlled trials from systematic reviews of treatment of non-specific LBP in the latest issue of the Cochrane Library, issue 2, 2005 and available databases until December 2005. Extracted data were effect sizes estimated as Standardized Mean Differences (SMD) and Relative Risk (RR) or data enabling calculation of effect sizes. For acute LBP, the effect size of non-steroidal anti-inflammatory drugs (NSAIDs) and manipulation were only modest (ES: 0.51 and 0.40, respectively) and there was no effect of exercise (ES: 0.07). For chronic LBP, acupuncture, behavioral therapy, exercise therapy, and NSAIDs had the largest effect sizes (SMD: 0.61, 0.57, and 0.52, and RR: 0.61, respectively), all with only a modest effect. Transcutaneous electric nerve stimulation and manipulation had small effect sizes (SMD: 0.22 and 0.35, respectively). As a conclusion, the effect of treatments for LBP is only small to moderate. Therefore, there is a dire need for developing more effective interventions.
Verkstedet Bodywork & Breathing System 