Pdf foredrag om alle faktorer som styrer pustefrekvensen.
Klikk for å få tilgang til Lec%208%202013%20Control%20of%20Breathing.pdf
Stikkordarkiv: Stress
A meta-ethnography of patients’ experience of chronic non-malignant musculoskeletal pain
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:
- an integrated relationship with the painful body
- redefining a positive sense of self now and in the future
- communicating to, rather than hiding from, others the experience of pain
- knowing that I am not the only one with pain (but I am still valued)
- regaining a sense of reciprocity and social participation
- recognising the limitations of the medical model
- being empowered to experiment and change the way that I do things without the sanction of the health-care professional.
Brain Mechanisms Supporting the Modulation of Pain by Mindfulness Meditation
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.
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).
Mindfulness starts with the body: somatosensory attention and top-down modulation of cortical alpha rhythms in mindfulness meditation
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.
Magnesium: Novel Applications in Cardiovascular Disease – A Review of the Literature
En review studie fra 2012 som inneholder det meste om Magnesium, spesielt rettet mot betennelser i hjerte/kar og nervesystemet.
http://www.karger.com/Article/FullText/339380
Magnesium L-lactate and L-aspartate are the oral magnesium compounds that have the greatest bioavailability, are the most water-soluble and have the greatest serum and plasma concentrations [8].
After a mean follow-up of 9.8 years and adjusting for confounders, the authors concluded that women in the highest quintile (an intake of 400 mg/day of magnesium) had a decreased HTN (hypertension) risk (p < 0.0001) versus those in the lowest quintile (approx. 200 mg/day of magnesium) [20].
Because of magnesium’s anti-inflammatory, statin-like and anti-mineralizing effects, a role for it is emerging in cardiovascular and neurological medicine.
The potential impact of magnesium in cardiovascular and neurological health, the abundance and low cost of the supplement, the relatively low side effect profile and the paucity of information in the literature about this common mineral suggest that more studies should be conducted to determine its safety and efficacy. The majority of human trials with magnesium thus far have not been interventional, but based on food questionnaires which may not be accurate and are subject to a recall bias. Further work is also needed to determine the mechanism of action by which magnesium modulates the mineralization and inflammation of the cardiovascular and nervous systems.
Neurogenic neuroinflammation: inflammatory CNS reactions in response to neuronal activity
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.
Stress and the inflammatory response: a review of neurogenic inflammation.
Betennelser kan både skapes og opprettholdes av nervesystemet.
Det er velkjent av betennelser økes av stresshormonet kortisol når vi stresser fordi kortisol senker immunfunksjon og dermed øker betennelsestilstander.
Men denne studien beskriver hvordan stress øker nevrogen betennelse (betennelse i nervesystemet), som kan forklare årsaken til at alt som vanligvis bare er litt ukomfortabelt blåses opp og blir vondere når vi er i langvarig stress.
Man tenker vanligvis på sansenerver som noe som sender signaler fra kroppen, gjennom ryggraden og opp til hjernen. Men molekyler kan faktisk gå andre veien i nervetrådene også. Fra ryggraden og UT i kroppen. Når vi stresser sender nervecellene ut et stoff som kalles Substans P, sammen med andre betennelsesøkende stoffer. Der hvor nervetrådene ender (i ledd, i huden eller i organer) blir det en lokal betennelsesreaksjon som bidrar til smerte. Substans P er spesielt assosisert med smertetilstander.
Forskeren konkluderer også med at dette er en viktig årsak til hvordan kronisk stress kan bidra til kroniske betennelsessykdommer som arterosklreose i blodårene eller betennelser i organene.
Beste måten å roe ned et stresset nervesystem er meditasjon med Autonom pust (5-6 pust i minuttet).
http://www.ncbi.nlm.nih.gov/pubmed/12480495
The subject of neuroinflammation is reviewed. In response to psychological stress or certain physical stressors, an inflammatory process may occur by release of neuropeptides, especially Substance P (SP), or other inflammatory mediators, from sensory nerves and the activation of mast cells or other inflammatory cells.
Central neuropeptides, particularly corticosteroid releasing factor (CRF), and perhaps SP as well, initiate a systemic stress response by activation of neuroendocrinological pathways such as the sympathetic nervous system, hypothalamic pituitary axis, and the renin angiotensin system, with the release of the stress hormones (i.e., catecholamines, corticosteroids, growth hormone, glucagons, and renin). These, together with cytokines induced by stress, initiate the acute phase response (APR) and the induction of acute phase proteins, essential mediators of inflammation. Central nervous system norepinephrine may also induce the APR perhaps by macrophage activation and cytokine release. The increase in lipids with stress may also be a factor in macrophage activation, as may lipopolysaccharide which, I postulate, induces cytokines from hepatic Kupffer cells, subsequent to an enhanced absorption from the gastrointestinal tract during psychologic stress.
The brain may initiate or inhibit the inflammatory process.
The inflammatory response is contained within the psychological stress response which evolved later. Moreover, the same neuropeptides (i.e., CRF and possibly SP as well) mediate both stress and inflammation.
Cytokines evoked by either a stress or inflammatory response may utilize similar somatosensory pathways to signal the brain. Other instances whereby stress may induce inflammatory changes are reviewed.
I postulate that repeated episodes of acute or chronic psychogenic stress may produce chronic inflammatory changes which may result in atherosclerosis in the arteries or chronic inflammatory changes in other organs as well.
Understanding the Process of Fascial Unwinding
Studie som nevner hvordan «fascial unwinding» skjer ved hjelp av stimulering av mekanoreseptorer i huden. Parasympatikus aktiveres og gjør at muskelspenninger slipper taket.
http://ijtmb.org/index.php/ijtmb/article/view/43/75
Hypothetical Model: During fascial unwinding, the therapist stimulates mechanoreceptors in the fascia by applying gentle touch and stretching. Touch and stretching induce relaxation and activate the parasympathetic nervous system. They also activate the central nervous system, which is involved in the modulation of muscle tone as well as movement. As a result, the central nervous system is aroused and thereby responds by encouraging muscles to find an easier, or more relaxed, position and by introducing the ideomotor action. Although the ideomotor action is generated via normal voluntary motor control systems, it is altered and experienced as an involuntary response.
Conclusions: Fascial unwinding occurs when a physically induced suggestion by a therapist prompts ideomotor action that the client experiences as involuntary. This action is guided by the central nervous system, which produces continuous action until a state of ease is reached. Consequently, fascial unwinding can be thought of as a neurobiologic process employing the self-regulation dynamic system theory.
In this paper, I propose a model based on scientific literature to explain the process and mechanism of fascial unwinding (Fig. 1). The model is based on the theories of ideomotor action by Carpenter(18) and Dorko,(16) fascia neurobiologic theory by Schleip,(4,5) and the psychology of consciousness by Halligan and Oakley.(19)
A set of conditions are required to initiate or facilitate the unwinding process. The therapist’s sensitivity and fine palpation skills form the most important part of these conditions, but it is also imperative that the client be able to relax and “let go” of his or her body.
In the first stage—the initiation or induction phase— the therapist working on a client will introduce touch or stretching onto the tissue. Touch is the entrance requirement for the process of unwinding. Touch stimulates the fascia’s mechanoreceptors and, in turn, arouses a parasympathetic nervous system response.(5) As a result of this latter response, the client is in a state of deep relaxation and calm, sometimes followed with rapid eye movement, twitching, or deep breathing—a state that can be observed clinically.(20,21) In this state, the conscious mind is relaxed and off guard. Stimulation of mechanoreceptors also influences the central nervous system. The central nervous system responds to this proprioceptive input by allowing the muscles to perform actions that decrease tone or that create movement in a joint or limb, making it move into an area of ease. At this point, ideomotor reflexes occur. Ideomotor action pertains to involuntary muscle movement, which can manifest in various ways and is directed at the central nervous system.(22)
These reflexes occur unconsciously, indicating dissociation between voluntary action and conscious experience.(23) In clinical situations, the client is unaware of the unconscious movement and thinks that it is generated by the therapist. This unconscious movement or stretching sensation stimulates a response in the tissue, providing a feedback to the central nervous system as outlined in the theory of ideomotor action.(24) The process is repeated until the client is relaxed or has reached a “still point” or state of ease.
The indirect stimulation of the autonomic nervous system (that is, the parasympathetic nervous system), which results in global muscle relaxation and a more peaceful state of mind, represents the heart of the changes that are so vital to many manual therapies. Gentler types of myofascial stretching and cranial techniques have also long been acknowledged to affect the parasympathetic nervous system.(25) Bertolucci(20) observed that, when a client is being treated with a muscle repositioning technique, the client begins to show involuntary motor reactions—reactions that include the involuntary action of related muscles and rapid eye movements. Several studies have evaluated the physiologic changes in the autonomic nervous system that occur as a result of craniosacral and MFR interventions,(21,26) clinically-known techniques that can trigger the unwinding process.
Recent studies have used heart rate variability, respiratory rate, skin conductance, and skin temperature as measures of physiologic change. Zullow and Reisman(26) indicated an increase in parasympathetic activity resulting from the compression of the fourth intracranial ventricle (CV4) maneuver and sacral holds, as measured by heart rate variability. Using heart rate variability measurement, Henley et al.(25) demonstrated that cervical MFR shifts sympathovagal balance from the sympathetic to the parasympathetic nervous system.
Dorko(16) was the first to suggest that fascial unwinding can be simply explained as an ideomotor movement. McCarthy et al.(29) were the first to document unwinding as an ideomotor-based manual therapy in the treatment of a patient with chronic neck pain. Their research showed that a reduction in pain intensity and perceived disability can be achieved with the introduction of ideomotor treatment.
A model built upon the neurobiologic, ideomotor action, and consciousness theories is proposed to explain the mechanism of unwinding. Touch, stretching, and manual therapy can induce relaxation in the parasympathetic nervous system. They also activate the central nervous system, which is involved in the modulation of muscle tone as well as movement. This activation stimulates the response to stretching: muscles find areas and positions of ease, the client experiences less pain or is more relaxed, thereby introducing the ideomotor action. The ideomotor action is generated through normal voluntary motor control systems, but is altered and experienced as an involuntary reaction. The stretching sensation provides a feedback to the nervous system, which in turn will generate the movements again.
How to make stress your friend
Spennende perspektiv på stress. Nevner at de som trodde at stress var farlig, hadde større sjanse for å dø av det. De som trodde stress ikke var farlig, hadde samme dødelighet som alle andre. Å vite hva stress er kan redde liv. Så neste gang du opplever stress, vit at «dette er kroppen min som hjelper meg å løfte energien til det nivået jeg trenger for å løse problemet», som hun sier i foredaget. Men gi også kroppen mulighet til å ta seg ned noen nivåer igjen når stresset er ferdig.
A new view on hypocortisolism
Om lavt kortisol-nivå og at det har en beskyttende effekt på kroppen etter langvarig høyt kortisol-nivå. En ny måte å se det på. Det er faktisk en overlevelsesmekanisme. Hvis vi ikke greier å skru av stresset eller fjerne oss fra den stressende livssituasjonen, vil kroppen etter hvert skru av stressresponsen og vi blir oversensitive for enhver utfordring. Utmattelse, muskelsmerter og fibromyalgi blir resultatet. Men likevel er det bedre for organismen enn videre stressresons. Studien forteller hvordan kortisol påvirker sentralnervesystemet, immunsystemet, oppvåkningsresponsen om morgenen, sickness responce, allostatic load, m.m.
http://cfids-cab.org/cfs-inform/Hypotheses/fries.etal05.pdf
Low cortisol levels have been observed in patients with different stress-related disorders such as chronic fatigue syndrome, fibromyalgia, and post- traumatic stress disorder. Data suggest that these disorders are characterized by a symptom triad of enhanced stress sensitivity, pain, and fatigue.
We propose that the phenomenon of hypocortisolism may occur after a prolonged period of hyperactivity of the hypothalamic–pituitary– adrenal axis due to chronic stress as illustrated in an animal model. Further evidence suggests that despite symptoms such as pain, fatigue and high stress sensitivity, hypocortisolism may also have beneficial effects on the organism. This assumption will be underlined by some studies suggesting protective effects of hypocortisolism for the individual.
Since the work of Selye (1936), stress has been associated with an activation of the hypothalamic– pituitary–adrenal (HPA) axis resulting in an increased release of cortisol from the adrenal glands. In recent years, a phenomenon has been described that is characterized by a hyporespon- siveness on different levels of the HPA axis in a number of stress-related states. This phenomenon, termed ‘hypocortisolism’, has been reported in about 20–25% of patients with stress-related dis- orders such as chronic fatigue syndrome (CFS), chronic pelvic pain (CPP), fibromyalgia (FMS), post-traumatic stress disorder (PTSD), irritable bowel syndrome (IBS), low back pain (LBP), burn- out, and atypical depression (Griep et al., 1998; Heim et al., 1998, 2000; Pruessner et al., 1999; Gold and Chrousos, 2002; Gur et al., 2004; Roberts et al., 2004; Rohleder et al., 2004). When hypo- cortisolemic, all these disorders may share affiliated syndromes characterized by a triad of enhanced stress sensitivity, pain, and fatigue.
However, despite different definitions we know today that there is a considerable overlap between the disorders.
In the early 1990s, Hudson and colleagues were amongst the first addressing this issue. They published a study on the comorbidity of FMS with medical and psychiatric disorders in which they reported a higher prevalence of migraine, IBS, and CFS, as well as higher lifetime rates of depression and panic disorder in patients with FMS (Hudson et al., 1992).
Thus, numerous studies on male war veterans have reported an association between PTSD and symp- toms such as fatigue, joint pain, and muscle pain (Engel et al., 2000; Ford et al., 2001).
These alterations of HPA axis are determined by (1) a reduced biosynthesis or release of the respective releasing factor/hormone on different levels of the HPA axis (CRF/AVP from the hypothalamus, ACTH from the pituitary, or cortisol from the adrenal glands) accompanied by a subsequent decreased stimulation of the respective target receptors, (2) a hypersecretion of one secretagogue with a subsequent down-regulation of the respective target receptors, (3) an enhanced sensitivity to the negative feedback of glucocorti- coids, (4) a decreased availability of free cortisol, and/ or (5) reduced effects of cortisol on the target tissue, describing a relative cortisol resistance (Heim et al., 2000; Raison and Miller, 2003).
Several years ago we postulated that hypocortiso- lism/a hyporeactive HPA axis might develop after prolonged periods of stress together with a hyper- activity of the HPA axis and excessive glucocorti- coid release (Hellhammer and Wade, 1993). This proposed time course with changes in HPA axis activity from hyper- to hypocortisolism resembles the history of patients with stress-related disorders who frequently report about the onset of ‘hypo- cortisolemic symptoms’ (fatigue, pain, stress sen- sitivity) after prolonged periods of stress, e.g. work stress, infection, or social stress (Buskila et al., 1998; Van Houdenhove and Egle, 2004)
Thinking about the potential cause/reason for changes in HPA axis activity from hyper- to hypocortisolism one might consider the body’s self-adjusting abilities as an important factor. Self-adjusting abilities play a significant role in survival of the organism by counteracting the enduring increased levels of glucocorticoids, and protecting the organism against the possible dele- terious effects thereof.
Poten- tial mechanisms of the ‘HPA axis adjustment’ are (1) the down-regulation of specific receptors on different levels of the axis (hypothalamus, pitu- itary, adrenals, target cells), (2) reduced biosyn- thesis or depletion at several levels of the HPA axis (CRF, ACTH, cortisol) and/or (3) increased negative feedback sensitivity to glucocorticoids (Hellhammer and Wade, 1993; Heim et al., 2000).
The suppressed stress response after administration of dexamethasone demonstrates an increased sensi- tivity to glucocorticoid negative feedback on the level of the pituitary.
The duration, intensity, number and chronicity of stressors may further pronounce these effects. The low-dose dexamethasone test may be the most sensitive measure of this condition.
The HPA axis plays an important role in the regulation of the SNS. CRF seems to increase the spontaneous discharge rate of locus coeruleus (LC) neurons and enhances norepinephrine (NE) release in the prefrontal cortex (Valentino, 1988; Valentino et al., 1993; Smagin et al., 1995), whereas glucocorticoids seem to exert more inhibitory effects on NE release.
Glucocorticoids are the most potent anti-inflam- matory hormones in the body. They act on the immune system by both suppressing and stimulating pro- and anti-inflammatory mediators. While they promote Th2 development, for example by enhan- cing interleukin (IL)-4 and (IL)-10 secretion by macrophages and Th2 cells (Ramierz et al., 1996), they inhibit inflammatory responses and suppress the production and release of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF- alpha), IL-1 and IL-6 (see Franchimont et al., 2003).
An important role of glucocorticoids during stress is to suppress the production and activity of pro- inflammatory cytokines, thus restraining the inflammatory reaction and preventing tissue destruction (see McEwen et al., 1997; Ruzek et al., 1999; Franchimont et al., 2003).
Therefore, a hypocortisolemic stress response, as observed in patients with stress-related disorders, may result in an overactivity of the immune system in terms of increased inflammatory responses due to impaired suppressive effects of low cortisol levels (see Heim et al., 2000; Rohleder et al., 2004). This assumption is supported by studies reporting elevated levels of pro-inflammatory cytokines in patients with stress-related disorders such as PTSD, CFS, and FMS (Maes et al., 1999; Patarca-Montero et al., 2001; Thompson and Barkhuizen, 2003; Rohleder et al., 2004).
Assessing the cortisol awakening response in pregnant women, preliminary results from our laboratory suggest that women with higher daily stress load showed lower cortisol levels in the morning compared to women with normal to low daily stress load. This result suggests a possible prevention of harmful stimulatory effects of maternal cortisol on placental CRF, which plays a major role in the initiation of delivery (Rieger, 2005).
The term ‘sickness response’ refers to non-specific symptoms such as fatigue, increased pain sensi- tivity, depressed activity, concentration difficul- ties, and anorexia that accompany the response to infection (Hart, 1988; Maier and Watkins, 1998). Sickness behavior at the behavioral level appears to be the expression of a central motivational state that reorganizes the organism’s priority to cope with infectious pathogens (Hart, 1988).
Further evidence for the protective effects of the development of a hypocortisolism refers to the allostatic load index. The term ‘allostatic load’ was irstly introduced by McEwen and Stellar (1993) describing the wear and tear of the body and brain resulting from chronic overactivity or inactivity of physiological systems that are normally involved in adaptation to environmental challenge. Allostatic load results when the allostatic systems (e.g. the HPA axis) are either overworked or fail to shut off after the stressful event is over or when these systems fail to respond adequately to the initial challenge, leading other systems to overreact (McEwen, 1998). In this context, results of Hell- hammer et al. (2004) demonstrate a significantly higher allostatic load index in older compared to younger subjects with the exception of hypocorti- solemic elderly who had a comparable allostatic load to young people even though they scored far higher on perceived stress scales. Considering the fact that allostatic load has been associated with a higher risk for mortality, these data suggest that a hypocortisolemic response to stress may rather be protective than damaging.
Low cortisol levels in the case of pregnant women may protect the mother and the child against the risk of pre-term birth, which could be harmful for both of them. Similarly, low cortisol levels in those individuals who are repeatedly or continuously exposed to intense immune stimuli may be beneficial for health and survival.
Similarly, low cortisol levels in those individuals who are repeatedly or continuously exposed to intense immune stimuli may be beneficial for health and survival. Most strikingly, the demonstration of a low allostatic load index in hypocortisolemic subjects suggests that a down-regulation of the HPA axis in chroni- cally stressed subjects protects those subjects against the harmful effects of a high allostatic load index.
Verkstedet Bodywork & Breathing System 