Kategoriarkiv: Forskning og artikler

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Om alt som er galt med fysio

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Her er et fantastisk innlegg fra en fysioterapeut. Dette er så spot-on at han ble kalt inn på teppet av ledelsen på sitt undiversitet og forsøkt kneblet. De mente han burde ha ventet med å skrive slikt til han hadde minst 5 år mer erfaring. Noe som bare viser hvordan autoriteter mangler evne til fleksibilitet, og at såkalte evidensbaserte behandlingsformer ikke greier å tilpasse seg ny forskning. Fysioterapi henger 50 år etter. Jeg har samlet alle referansene for lettere tilgang.

http://blog.theravid.com/patient-care/redefining-evidence-ebp-in-experience-cut/

How does one justify the use of ultrasound when the biophysical (Baker et al 2001) and clinical (Robertson et al 2001) effects have been so thoroughly disproven?

Why are we still taught that we are molders of connective tissue, when the forces required to create plastic deformation of connective tissue ranges between 50 and 250 pounds of force (Threlkeld 1992)?

When are we going to accept the fact that our palpatory exams lack reliability (French et al 2000) (Lucas et al 2009)

and validity (Najm et al 2003) (Landel et al 2008) (Preece et al 2008)?

When will we stop telling students, colleagues, and patients that pain is related to their posture, muscle length, muscle strength, or biomechanics (Edmondston et al 2007) (Lewis et al 2005) (Nourbakhsh et al 2002)?

When will we cease blaming pain on something found on an image (Reilly et al 2006) (Beattie et al 2005) (Borenstein et al 2001)?

When will we stop thinking that we can change someone’s static posture with strengthening (Walker et al 1987) (Diveta et al 1990)?

When we teach these things to students and say them to our patients, it is misleading at best and fear inducing and hurtful at worst (Zusman 2012).

“In My Experience”remain the three most dangerous words in medicine.

This is perhaps even doubly so in the world of physical therapy, given the litany of non-specific effects that go into a treatment encounter (Hall et al 2010) (Miciak et al 2012).

Physical therapists are in a unique position to make a significant impact on the burden of chronic pain, however, we fail to live up to our potential by holding onto a postural-structural-biomechanical model that has been proven ineffective and incorrect (Lederman 2011).

We need to familiarize ourselves with the work of people like Ronald Melzack, Patrick Wall, Louis Gifford, David Butler and Lorimer Moseley.

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Skin Biopsy as a Diagnostic Tool in Peripheral Neuropathy: Correlates of Intraepidermal Nerve Fiber Density

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Denne nevner mye om nevropati og sammenhengen mellom small fiber density og smerte, pluss at den nevner hvordan trening og steroidbehandling øker tettheten igjen. Viktigst prinsipp å hente fra denne artikkelen er at c-fiber tettheten sier noe om intensiteten på smerten, men ikke noe om smertetilstanden. Man kan ha lav tetthet og lite smerte, men om man får smerte er intensiteten desto høyere. Man må desverre logge inn for å få opp linkene.

http://www.medscape.org/viewarticle/563262_6

In diabetic neuropathy, patients with pain had lower IENF densities than did asymptomatic patients, but IENF density did not correlate with pain intensity within the group of symptomatic patients.[82]

In patients with impaired glucose tolerance, diet and exercise induced a slight recovery of IENF density that was associated with a reduction in pain symptoms.[83] Similarly, epidermal reinnervation coincided with pain reduction after steroid treatment.[71]

CORRELATES OF INTRAEPIDERMAL NERVE FIBER DENSITY

Clinical Picture, Etiology and Neuropathic Pain

The clinical picture of small-fiber neuropathy is dominated by spontaneous and stimulus-evoked positive sensory symptoms—namely thermal and pinprick hypoesthesia—that can mask the signs of small-fiber loss. Only a few studies have attempted to correlate IENF density with validated clinical scales. In patients with diabetic neuropathy, a negative correlation between IENF density and neuropathy symptom score was reported.[53,56]These studies also showed that the extent of epidermal denervation correlated with the duration of diabetes but not with hemoglobin A1C levels, suggesting that IENF density might be useful as a marker of neuropathy progression. A recent study found a high concordance between reduced IENF density and loss of pinprick sensation in the foot.[61]

Skin biopsy has allowed small-fiber neuropathy to be demonstrated in restless legs syndrome[75] and erythromelalgia.[76] In systemic diseases, such as systemic lupus erythematosus, sarcoidosis, Sjögren’s syndrome, celiac disease and hypothyroidism, skin biopsy has enabled correlations to be found between neuropathic symptoms and small-fiber degeneration.[52,65,77–79]Although IENF density is a general marker of axonal integrity in peripheral neuropathies, it cannot be used to directly address the question of etiology. Skin biopsy findings can, however, indirectly contribute to the assessment of etiology. For example, in 40% of patients with small-fiber neuropathy diagnosed only after skin biopsy, oral glucose tolerance testing revealed a previously undetected impaired glucose tolerance.[49] Similarly, the distribution of IENF loss can help to differentiate between a non-length-dependent sensory neuronopathy and a length-dependent axonal neuropathy,[78,80] thereby leading to focused screening for associated diseases.

The relationship between IENF density and neuropathic pain remains uncertain. In HIV neuropathy, IENF density correlated inversely with pain severity when assessed by the patient, but not when the Gracely Pain Scale was used.[66] Another study found only a trend towards an inverse correlation between IENF density and pain intensity in this setting.[81] In diabetic neuropathy, patients with pain had lower IENF densities than did asymptomatic patients, but IENF density did not correlate with pain intensity within the group of symptomatic patients.[82] In patients with impaired glucose tolerance, diet and exercise induced a slight recovery of IENF density that was associated with a reduction in pain symptoms.[83] Similarly, epidermal reinnervation coincided with pain reduction after steroid treatment.[71]In length-dependent neuropathies, therefore, more-severe IENF loss seems to increase the risk of developing pain, the intensity of which might decrease in parallel with recovery of IENF density.

In postherpetic neuralgia, on the basis of evidence of relatively preserved skin innervation in the area of severe allodynia, normal thermal sensory function, pain relief in response to topical lidocaine, and worsening of pain with application of capsaicin, surgical removal of painful skin has been attempted.[84] After initial relief, pain increased, became intractable, and spread to previously unaffected dermatomes, suggesting the involvement of central mechanisms in the pathogenesis of neuropathic pain.

Sensory Nerve Conduction Studies

Sural sensory nerve action potential (SNAP) amplitude, which reflects the integrity of largediameter fibers, showed concordance with IENF density in the distal part of the leg in patients with large-fiber or mixed small-fiber and largefiber neuropathy. Not surprisingly, skin biopsy analysis seemed to be more sensitive than sural nerve conduction studies for diagnosing smallfiber neuropathy.[62] One study,[85] however, showed that in patients with symptoms of small-fiber neuropathy and normal sural nerve conduction, reduced IENF density correlated with a decrease in SNAP amplitude in the medial plantar nerve. This finding suggests subclinical involvement of the most-distal large fibers in small-fiber neuropathy.

Psychophysical Tests

The detection of thermal and pain thresholds using quantitative sensory testing has been widely used to assess the function of small nerve fibers. Although this approach is useful in population studies, it is an unreliable tool for diagnosing small-fiber neuropathy in clinical practice.[86] Moreover, the size of the probe used for the test can affect the results.[87]

In view of the fact that unmyelinated fibers and thinly myelinated fibers convey warm and cold sensation, respectively, thermal thresholds would be expected to correlate with IENF density. In diabetic neuropathy, IENF density was found to be inversely correlated with thermal and pain thresholds, showing the highest correlation with warm threshold.[53,56,82]Similarly, in Guillain–Barré syndrome lower IENF density was associated with increased warm threshold.[67]One study reported a significant correlation between cold pain threshold and signs of large-fiber impairment.[59]By contrast, others studies did not find any correlation between quantitative sensory testing results and IENF density.[45,51,88]

Autonomic Tests

As IENFs are somatic unmyelinated fibers, their density would not be expected to correlate with autonomic fiber function. Intriguingly, however, in patients with Guillain–Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy, lower IENF density was associated with a higher risk of developing dysautonomia.[64,67]These findings suggest that the integrity of IENFs might reflect the integrity of the whole class of small nerve fibers, including autonomic fibers. A few studies have investigated the correlation between IENF density and the results of a quantitative sudomotor axonal reflex test in patients with painful neuropathy and autonomic symptoms in order to test the hypothesis that IENF density and sweat output might decrease concomitantly. IENF density correlated with test results in one study,[63] but not in another.[51] In leprosy neuropathy, reduced nicotine-induced axon-reflex sweating correlated with decreased innervation of sweat glands.[88]

Nonconventional Neurophysiological Tests

Laser-evoked potentials (LEPs) have been used to investigate peripheral and central nociceptive pathways in trigeminal neuralgia and peripheral neuropathies. Late LEPs, reflecting Aδ-fiber activation, are delayed in patients with neuropathic pain, but can be enhanced when the pain has a psychogenic origin.[89] Recording of ultralate LEPs, reflecting activation of unmyelinated C-fibers, is less reliable than recording of late LEPs, thereby limiting the overall usefulness of LEPs in clinical practice. LEPs and skin biopsy findings have been examined in single case reports.[90]In two patients with Ross syndrome, abnormal LEPs correlated with decreased IENF density and increased thermal thresholds.[91] No study has yet looked for a correlation between results of skin biopsy analysis and recording of contact heat-evoked potentials, a technique that was recently proposed for investigating smallfiber function, but which cannot be used to assess C-fiber-related responses.[92]

Microneurography allows single-fiber recordings from nerves in awake patients. This technique demonstrated loss of nociceptive and skin sympathetic C-fiber activity that correlated with IENF and sweat gland denervation in a patient with hereditary sensory and autonomic neuropathy type IV.[20]In two patients with generalized anhidrosis, C-fiber recording and sweat gland innervation analysis distinguished postganglionic autonomic nerve fiber impairment from eccrine gland dysfunction.[34]

Sural Nerve Biopsy

The diagnosis of small-fiber neuropathy is better assessed by skin biopsy than by sural nerve biopsy.[57]IENF density can be reduced despite normal morphometry of unmyelinated and thinly myelinated fibers in sural nerve biopsy.[58] In a large comparative study,[62] skin and sural nerve biopsy findings were concordant in 73% of patients, but in 23% of patients IENF density was the only indicator of small-fiber neuropathy. Skin biopsy offers the opportunity to differentiate small nerve fibers with somatic function from those with autonomic function, thereby giving it a further advantage over nerve biopsy. In Charcot–Marie–Tooth disease and related hereditary neuropathies, a biopsy sample of the glabrous skin demonstrated the typical neuropathological abnormalities known from sural nerve studies.[5,6]

Immunohistochemical studies demonstrated IgM deposited specifically in the myelinated fibers of hairy and glabrous skin in patients with anti-myelin-associated-glycoprotein neuropathy.[93] Although skin biopsy can be contemplated in genetic and immune-mediated neuropathies, sural nerve biopsy should always be considered to confirm the diagnosis in inflammatory polyradiculoneuropathy with atypical presentation, or when vasculitic or amyloid neuropathy is suspected.

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High spontaneous activity of C-nociceptors in painful polyneuropathy.

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Viser hvordan c-fibre fyrer av i både smertefull og ikke-smertefull nevropati. Jo mer spontan aktivitet c-fibrene har, jo mer smerte oppleves.

http://www.ncbi.nlm.nih.gov/pubmed/22986070?dopt=Abstract

Polyneuropathy can be linked to chronic pain but also to reduced pain sensitivity. We investigated peripheral C-nociceptors in painful and painless polyneuropathy patients to identify pain-specific changes. Eleven polyneuropathy patients with persistent spontaneous pain and 8 polyneuropathy patients without spontaneous pain were investigated by routine clinical methods

The mean percentage of C-nociceptors being spontaneously active or mechanically sensitized was significantly higher in patients with pain (mean 40.5% and 14.6%, respectively, P=.02). The difference was mainly due to more spontaneously active mechanoinsensitive C-nociceptors (operationally defined by their mechanical insensitivity and their axonal characteristics) in the pain patients (19 of 56 vs 6 of 43; P=.02).

Hyperexcitability in mechanoinsensitive C-nociceptors was significantly higher in patients with polyneuropathy and pain compared to patients with polyneuropathy without pain, while the difference was much less prominent in mechanosensitive (polymodal) C-nociceptors. This hyperexcitability may be a major underlying mechanism for the pain experienced by patients with painful peripheral neuropathy.

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Double spikes to single electrical stimulation correlates to spontaneous activity of nociceptors in painful neuropathy patients.

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Viser hvor stor andel av c-fibrene som har spontan aktivitet ved nevropati, og hvor stor andel av de igjen som har dobbelt eller trippelt avfyring. Nevner at spontane avfyringer skjer i en viss andel av de uten multippel avfyring også. Og at selv uten smerte er det en liten andel av fibrene som fyrer av dobbelt. De konkluderer med at det er usikkert hvordan slik spontan aktivitetet egentlig er relatert til kliniske smertenivåer.

http://www.ncbi.nlm.nih.gov/pubmed/22154219

Multiple firing of C nociceptors upon a single electrical stimulus has been suggested to be a possible mechanism contributing to neuropathic pain. Because this phenomenon maybe based on a unidirectional conduction block, it might also be related to neuropathic changes without a direct link to pain.

In 11 of 105 nociceptors, double spiking was found, with 1 fibre even showing triple spikes on electrical stimulation.

There was a significant association between spontaneous activity and multiple spiking in C nociceptors, with spontaneous activity being present in 9 of 11 fibres with multiple spiking, but only in 21 of 94 nociceptors without multiple spiking (P<.005, Fisher exact test).

Among the 75 C nociceptors without spontaneous activity, only 2 nociceptors showed multiple spiking.

In 8 neuropathy patients without pain, double spiking was found only in 4 of 90 nociceptors

Multiple spiking of nociceptors coincides with spontaneous activity in nociceptors of painful neuropathy patients. We therefore conclude that rather than being a generic sign of neuropathy, multiple spiking is linked to axonal hyperexcitability and spontaneous activity of nociceptors. It is still unclear whether it also is mechanistically related to the clinical pain level.

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Double and triple spikes in C-nociceptors in neuropathic pain states: an additional peripheral mechanism of hyperalgesia.

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Om at nociceptive c-fibre i en nevropatisk tilstand kan fyre av dobbelt og trippelt ved en enkel stimulering. De forsterker signalene og bidrar til hyperalgesi (økt smerteopplevelse av en vanligvis normal smerteaktivering).

http://www.ncbi.nlm.nih.gov/pubmed/21130572

It was previously reported that in 5 patients with small-fiber neuropathy, neuropathic pain, and hyperalgesia, application of a single, brief electrical stimulus to the skin could give rise to 2 afferent impulses in a C-nociceptor fiber. These double spikes, which are attributed to unidirectional conduction failure at branch points in the terminal arborisation, provide a possible mechanism for hyperalgesia.

We here report that similar multiple spikes are regularly observed in 3 rat models of neuropathic pain: nerve crush, nerve suture, and chronic constriction injury. The proportion of nociceptor fibers exhibiting multiple spikes was similar (10.1-18.5%) in the 3 models, and significantly greater than the proportion in control (unoperated) animals (1.2%).

Whereas only double spikes had previously been described in patients, in these more extensive recordings from rats we found that triple spikes could also be observed after a single electrical stimulus. The results strengthen the suggestion that multiple spiking, because of impaired conduction in the terminal branches of nociceptors, may contribute to hyperalgesia in patients with neuropathic pain. Double and triple spikes in c-nociceptors, caused by impaired conduction in terminal branches, may be an important cause of hyperalgesia in patients with neuropathic pain.

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The Puzzle of Pelvic Pain: A Rehabilitation Framework for Balancing Tissue Dysfunction and Central Sensitization II: A Review of Treatment Considerations

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Om pelvic pain, en tilstand som mange opplever men som er vanskelig å behandle når man mangler elementer fra smertefroståelse. Dette gjelder egentlig alle kroniske smertetilstander. Alt forklares i denne viktige studien. Nevner biomedicinalism, ny forståelse av smerte, sentral sensitering, body maps, graded motor imagery, mirror therapy, m.m. Behandlingskonseptet som nevnes ligner det vi har etablert på Verkstedet.

http://www.thepelvicmessenger.org/upload/The_Puzzle_of_Pelvic_Pain___A_Rehabilitation.5.pdf
Physical therapists have been instrumental in guiding the medical system away from “end-organ” focus in the assessment and treatment of persistent pelvic pain. How- ever, for the most part physical therapists remain in a bio- medical model of treatment focusing on tissue dysfunction as a framework for the assessment and treatment of per- sistent pelvic pain. This article proposes a framework that integrates current understanding of local tissue dysfunc- tion with the wider context of sensitized protective mecha- nisms within the spinal cord and brain. Current concepts in pain science, particularly as it relates to the Neuromatrix and central sensitization, lead away from bio-medicalism towards a bio-psycho-social model of evaluation and treat- ment of persistent pelvic pain.

They proposed a framework for the treatment of pelvic floor dysfunction that moved away from the traditional strengthening approach of Kegel exercises. The idea that one cause of persistent pelvic pain and overactive bladder syndromes may be hypertonic muscles, instead of hypotonic muscles, has changed the treatment focus for some patient complaints of pelvic pain.

Physical therapists have made a compelling argument that many forms of persistent pelvic pain may have origins in myofascial dysfunction causing “end point” organ irritation, including swelling, redness, and pain in the bladder, prostate, testicles, or the vagina.4

Fitzgerald et al5 demonstrated in a multicenter feasibility study that physical therapy intervention of myofascial treatment applied to the perineum, abdominal wall, and pelvic floor demonstrated a 57% response rate compared with a 21% improvement rate with general massage therapy.

Butler7 describes biomedicalism as a “patho-anatomical search for a singular cause for chronic problems.” Waddel8 defines a biopsychosocial approach as an “individual-centered model that considers the person, their health problem and their social context.” The International Association for the Study of Pain describes pain as a “sensory and emotional experience”9 that encompasses both tissue nociception and the inter- pretation of the pain experience.

Globally, chronic pain and stress are at epidemic levels, as history shows, epidemics are best altered by education.7 The treatment of chronic pelvic pain has been well-recognized to have a mind (stress)- body (nociception) connection; however, education has not been widely used in this pain population to effectively link the 2 areas.

The summary of these conceptual changes is as follows:

  1. Pain is an output expression of the brain in response to a perception of threat.14,15 A therapeu- tic goal in persistent pain is to restore movement without triggering a protective pain response.
  2. Pelvic pain is complex. Psychosocial considerations include sexuality, cultural expectations, privacy, and religious issues.
  3. Chronic pain does not necessarily correlate with injury or disease, and nociception is neither neces- sary nor sufficient for a pain response.15,16
  4. The nervous system slides and glides as we move.16-18
  5. Neurophysiology-based pain education is an effec- tive adjunct to physical therapy intervention.12,13,19 Educating patients in the concepts of pain science, including neural plasticity, increases understanding and decreases the threat response.

Central sensitization encompasses “impaired functioning of brain-orchestrated descend- ing anti-nociceptive (inhibitory) mechanisms and (over) activation of descending and ascending pain facilitatory pathways.”21 The pain response operates within the entire system of nociceptive input, periph- eral neurogenic sensitization, and central sensitiza- tion.

Neurophysiology-based pain education forms the basis of treatment in central sensitization and refers to patient education about the role of central and peripheral processes in persistent pain.21 A patient who believes that local tissue dysfunction is the primary cause of a chronic pain state is likely to have thoughts and beliefs that limit normal mobility and function in the affected area.30

There are a mas- sive number of potential threats within the context of persistent pain.30 Using educational tools in the clinic to accurately explain pain helps give contextual meaning to the patient’s symptoms. Reduction of threat decreases the need for the engagement of active coping systems such as the sympathetic, immune, endocrine, and motor systems and the need for pro- tective pain states.16,38 Threats can be identified in a biopsychosocial framework (Table 1).

Table 1. Identifying Threats in a Biopsychosocial Frameworka

Biological
Worried x-rays showing “arthritis” Worried x-rays showing disc bulges Lack of specific diagnosis
Multiple medications ineffective Doing too much without pacing

Psychological
Fear of pain
Fear of not recovering
Fear of serious injury
Fear of reinjury Sadness/depression Hopelessness about recovery Attitude toward sexuality

Social
Withdrawn from family/joy Withdrawn from hobbies/sports Legal battle stress
Family stress/anger
Financial stress/worries
Work stress/anger

When sensitized neural states have been identified, the use of neurophysiology of pain education then flows into gentle guided exercises to normalize input into the sensory-motor cortex. Within the neuroma- trix, there are sensory maps, motor maps, and maps for smell, vision, and peripersonal space to name a few.39 The smudging of these body maps refers to a loss of normally distinctive localization and has been demonstrated in phantom limb pain,40,41 complex regional pain syndrome (CRPS),42 and chronic pain.43 Smudging in the sensory-motor cortex often occurs in the painful area and can also occur in the body part adjacent to the affected area on the homunculus.41,43

Patients with pelvic pain may report symptoms that could be indicative of smudging including the sensa- tion that their pelvic anatomy is altered or missing, or they may report foot pain that began after their pelvic pain. Since the feet lie next to the genitals on the homunculus, it is postulated that this may be the result of homuncular smudging.

Gentle guided movements such as pelvic tilts, move- ment of the ischial tuberosities, and guided sensory training in various sitting, standing, and lying postures may be useful for increasing sensory awareness.47,48

Body map training may be used to address the neuromatrix by modifying fear con- ditioning, teaching neutral alignment, reorganizing the sensorimotor cortex, and changing awareness of body parts.39,40,51

There are approximately 200 inhibitory neurons descending from the brain that help downregulate the sensitive nervous system for every one nocicep- tive or danger neuron traveling up to the brain.16

The activity in descending pathways is not constant and can be modulated.52 Decreasing levels of vigilance, attention, and stress are some techniques that may enhance the activity in the descending pathways.12,21 Decreasing a stress response may also help to decrease the sympathetic nervous system response.

Treatment options may include the following:
• Connective tissue mobilization: Mobilization of the soft tissue is used to have a direct effect on tis- sue dysfunction, given the basic need of muscles, fascia, and neural tissue to move in order to be healthy.3,53 Connective tissue mobilization may also directly impact the state of the autonomic nervous system, specifically by interrupting the viscera-somatic reflex arc, which is an autonomic reflex.54 Therefore, connective tissue mobilization may affect both tissue dysfunction and sensitiza- tion through modulation of the nervous system. Clinically, treatment of the connective tissue has been shown to be an important component of tissue dysfunction-based treatment in urologically based pelvic pain.5 It is proposed that this treat- ment may have an important effect not only on local tissue dysfunction but also on the sensitized nervous system.
• Deep breathing: Oxygen is vital for every organ in our body. People with persistent pain tend to have maladaptive breathing patterns, including shallow apical breathing.55 Retraining deep breathing, with both lateral costal and diaphragmatic techniques, is believed to downregulate the sensitive ner- vous system, particularly the sympathetic nervous system.55

• Relaxation training: There are many different styles of relaxation training, including paradoxical relaxation,24 progressive muscle relaxation, auto- genic training, mindfulness training, and medita- tion.56 Research shows that people who meditate have more gray matter in regions of the brain that are important for attention, emotional regu- lation, and mental flexibility.55 Meditation may also decrease anxiety and improve self-esteem.57 Mindfulness training is the skill of maintaining focus on something by choice while allowing thoughts, emotions, and sensations to come in and out of awareness, and at the same time, aware- ness without judgement.56 Patients will respond to different relaxation strategies and a variety of relaxation strategies should be tried to find the best fit. Clinically, patients will gravitate to one form or another, often from personal preference. Allowing a patient to choose her or his preference may help improve compliance.58
• Cardiovascular exercise: There is evidence that aerobic exercise lowers a person’s stress response and assists in mood and anxiety relief.59,60 The American College of Sports Medicine recommends performing moderately intense cardiovascular exercise for 30 minutes per day on at least 5 days per week, or vigorously intense cardiovascular exercise for 20 minutes per day on at least 3 days a week. In addition, the recommendation is that an individual perform 8 to 12 repetitions of 8 to 10 strength training exercises at least twice per week.61
• Guided imagery: Guided imagery allows for individual exploration into belief patterns and movement patterns that may not be helpful in the goal of returning to normal movement and function. These thoughts, beliefs, and move- ments are often outside of conscious awareness and largely outside of one’s control.62 Imagery engages the power of the mind to reduce anxiety, depression, and stress. Carrico et al62 conducted a pilot study, using a guided imagery CD spe- cifically recorded and scripted for women with interstitial cystitis and pelvic pain. The study found that approximately 45% of the treat- ment group participants responded to guided imagery therapy, noting a moderate or marked improvement on the global response assessment. Pain scores and episodes of urgency significantly decreased in the treatment group.

• Yoga: The term yoga is derived from the Sanskrit verb yug, which means to bind or join. This refers to the overarching goal of yoga to unite the mind and body in a way that promotes health.63 Comprehensive protocols have been adapted for yoga in the management of chronic pain. Yoga specifically addresses body awareness through body map training, breathing techniques, and increased awareness of mental and physical states, which may help patients better understand their pain response. Several mechanisms could potential- ly explain the benefits of yoga for persistent pain conditions. Yoga can decrease sympathetic ner- vous system activity, reduce inflammatory mark- ers, reduce stress markers (cortisol), and increase flexibility, strength, circulation, and cardiorespi- ratory capacity.63 Yoga has also been shown to increase the frequency of positive emotions and could potentially undo the physiological effects of negative emotions, broaden cognitive processes, and build physical and psychological resources.63 Finally, it is possible that yoga can lead to improve- ments in self-efficacy for pain control.63
• Affirmations/positive thinking: Patients may be able to learn to control and change their thoughts, seeking mastery in the following areas: stress inoculation, assertiveness in dealing with their sit- uation, handling conflict that arises around their pain, and decreasing their resistance to get bet- ter.64 Thoughts are nerve impulses, and negative thinking alone may drive persistent pain states. Moseley et al65 demonstrated that the thought of movement alone was sufficient to increase pain and swelling in CRPS. The contribution to persis- tent pain states from thoughts and beliefs provides a significant possibility for therapeutic interven- tion. Clinicians can assist and encourage the use of positive affirmations and can demonstrate good modeling of these techniques.
• Joy/laughter: Ongoing stress, particularly in the absence of positive coping skills, lowers resistance, weakens the immune system, and increases suscep- tibility to health problems.66 Pain is reduced while undergoing functional magnetic resonance imag- ing by positive pictures, beautiful music, positive expectations, enticing smells, sweet tastes, social touch, and sexual behavior.67 Patient instruction may include choosing a positive environment for exercise, one that is interesting, novel, and fun.

• Addressing sleep dysfunction: A systematic review concluded that there is consistent evidence asso- ciating chronic low back pain with greater sleep disturbances and reduced sleep duration.68 Reid et al69 looked at the efficacy of aerobic physical activity with sleep hygiene education to improve sleep, mood, and quality of life in individuals with chronic insomnia. The study concluded that an aerobic physical exercise program (involving two 20-minute sessions 4 times per week or one 30-minute session 4 times per week) with sleep hygiene education can be very beneficial to patients with insomnia and depressive mood.69

In peripheral neurogenic pain, nerves are sensitized as a result of plastic changes that have occurred within the peripheral nervous system, including the development of abnormal impulse-gen- erating sites.16,17,71-73 Nerves may also be sensitized because of chemical processes from proinflammatory mediators including prostaglandins, serotonin, brady- kinin, cytokines, and macrophages.16,74

Decreasing the sensitivity of the peripheral nerves may be addressed mechanically through a variety of manual therapy techniques that propose to unload the nerve by increasing the space or fluid motion in the tis- sues around the nerve.2,17,18,24 With decreased tension of the soft tissues surrounding the nerves including muscles, connective tissue, scar tissue, and abnormal joint mechanics, the nerve has a better chance of moving well within the space surrounding it.

A neurodynamic assessment includes physical pal- pation of the nerve where possible, as well as passive and active neurodynamic tests.16,70 For the pelvis, this involves the pudendal, ilioinguinal, iliogastric, femoral, and obturator branches of the lumbosacral nerves.

The pudendal nerve can also be mobilized through various depths of squatting with modifying the neck position to load and unload the dura mater and the nervous system. (See Appendix A.)

Once tissue dysfunction, central sensitization, and neurodynamics have been addressed and are showing signs of improvement, patients need to establish short- and long-term goals to help reduce the threat of increased function. The patient may be asked to create a list of pain control strategies that they can use to pace activities.

Hebb93 described the neurologic basis of motor learning as “Neurons that fire together, wire together. Neurons that fire apart, stay apart.” This is the key concept in using graded motor imagery in retraining the sensitive nervous system. By practicing the skill first through imagery and then progressing to actual movement, there is a change in the representation of the movement and the involved body parts in the sen- sory and motor cortices.46,94 Notably, this can be done without triggering a protective pain response that will help restore normal sensitivity to the nervous system.

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Objective evidence that small-fiber polyneuropathy underlies some illnesses currently labeled as fibromyalgia

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Om fibromyalgi og at 41% av pasientene har tynnfibernevropati. 3% av kontrollgruppen har det. Tynnfibernevropati-type smerter er en del av mange sykdommer og flere studier viser at det er underdiagnostisert.

http://www.painjournalonline.com/article/S0304-3959(13)00294-7/abstract

No specific objective abnormalities have been identified, which precludes definitive testing, disease-modifying treatments, and identification of causes.

We found that 41% of skin biopsies from subjects with fibromyalgia vs 3% of biopsies from control subjects were diagnostic for SFPN, and MNSI and UENS scores were higher in patients with fibromyalgia than in control subjects (all P⩽0.001).

Abnormal AFTs (autonomic function test) were equally prevalent, suggesting that fibromyalgia-associated SFPN is primarily somatic.

These findings suggest that some patients with chronic pain labeled as fibromyalgia have unrecognized SFPN, a distinct disease that can be tested for objectively and sometimes treated definitively.

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Deconstructing the Placebo Effect and Finding the Meaning Response

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Om placeboeffekten og at «mening» er bedre å bruke enn en placeborespons når vi snakker om behandling. Placebo-sukkerpillen har ingen effekt i kroppen, men meningen vi legger i den har det. Vi får en «meningsrespons». Selv medisiner eller operasjoner får bedre effekt når det er en «mening» bak det.

http://annals.org/article.aspx?articleid=715182

http://www.homeopathy.org/wp-content/uploads/downloads/2012/05/Mossman.pdf

We provide a new perspective with which to understand what for a half century has been known as the “placebo effect.” We argue that, as currently used, the concept includes much that has noth- ing to do with placebos, confusing the most interesting and im- portant aspects of the phenomenon. We propose a new way to understand those aspects of medical care, plus a broad range of additional human experiences, by focusing on the idea of “mean- ing,” to which people, when they are sick, often respond.

We review several of the many areas in medicine in which meaning affects illness or healing and introduce the idea of the “meaning response.” We suggest that use of this formulation, rather than the fixation on inert placebos, will probably lead to far greater insight into how treatment works and perhaps to real improvements in human well-being.

If we replace the word “placebo” in the second sentence with its definition from the first, we get: “The placebo effect is the therapeutic effect produced by [things] objectively without specific activity for the condition being treated.” This makes no sense whatsoever. Indeed, it flies in the face of the obvious. The one thing of which we can be absolutely certain is that placebos do not cause placebo effects. Placebos are inert and don’t cause anything.

Moreover, people frequently expand the concept of the placebo effect very broadly to include just about every conceivable sort of beneficial biological, social, or human interaction that doesn’t involve some drug well- known to the pharmacopoeia.

The concept of the placebo effect has been expanded much more broadly than this. Some attribute the effects of various alternative medical systems, such as homeopathy (33) or chiropractic (34), to the placebo effect. Others have described studies that show the positive effects of enhanced communication, such as Egbert’s (35), as “the placebo re- sponse without the placebo” (7). No wonder things are confusing.

Instead, they can be ex- plained by the “meanings” in the experiment: 1) Red means “up,” “hot,” “danger,” while blue means “down,” “cool,” “quiet” and 2) two means more than one. These effects of color (37– 40) and number (41, 42) have been widely replicated.

In this study, branded aspirin worked better than unbranded aspirin, which worked better than branded placebo, which worked better than unbranded placebo.

Aspirin relieves headaches, but so does the knowledge that the pills you are taking are “good” ones.

n a study of the benefits of aerobic exercise, two groups participated in a 10-week exercise program. One group was told that the exercise would enhance their aerobic capacity, while the other group was told that the exercise would enhance aerobic capacity and psychological well-being. Both groups improved their aerobic capacity, but only the second group improved in psychological well-being (actually “self-esteem”). The re- searchers called this “strong evidence . . . that exercise may enhance psychological well-being via a strong placebo effect” (44).

It seems reasonable to label all these effects (except, of course, of the aspirin and the exercise) as “mean- ing responses,” a term that seeks, among other things, to recall Dr. Herbert Benson’s “relaxation response” (45). Ironically, although placebos clearly cannot do anything themselves, their meaning can.

We define the meaning response as the physiologic or psychological effects of meaning in the origins or treatment of illness; meaning responses elicited after the use of inert or sham treatment can be called the “placebo effect” when they are desirable and the “nocebo effect” (46) when they are undesirable.

Insofar as medicine is meaningful, it can affect pa- tients, and it can affect the outcome of treatment (47– 49). Most elements of medicine are meaningful, even if practitioners do not intend them to be so. The physi- cian’s costume (the white coat with stethoscope hanging out of the pocket) (50), manner (enthusiastic or not), style (therapeutic or experimental), and language (51) are all meaningful and can be shown to affect the out- come; indeed, we argue that both diagnosis (52) and prognosis (53) can be important forms of treatment.

Likewise, acupuncture analgesia can be reversed with naloxone in animals (61) and people (62). To say that a treatment such as acupuncture “isn’t better than placebo” does not mean that it does nothing.

Surgery is particularly meaningful: Surgeons are among the elite of medical practitioners; the shedding of blood is inevitably meaningful in and of itself.

The intensity of the effect was shown to be correlated with “the strength of commitment to traditional Chinese culture.” These differences in longevity (up to 6% or 7% difference in length of life!) are not due to having Chinese genes but to having Chinese ideas, to knowing the world in Chinese ways. The effects of meaning on health and disease are not restricted to placebos or brand names but permeate life.

Practitioners can benefit clinically by conceptualizing this issue in terms of the meaning response rather than the placebo effect. Placebos are inert. You can’t do anything about them. For human beings, meaning is everything that placebos are not, richly alive and powerful.

One reason we are so ignorant is that, by focusing on placebos, we constantly have to address the moral and ethical issues of prescribing inert treatments (73, 74), of lying (75), and the like. It seems possible to evade the entire issue by simply avoiding placebos. One cannot, however, avoid meaning while engaging human beings. Even the most distant objects—the planet Venus, the stars in the constellation Orion—are meaningful to us, as well as to others (76).

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Neural tissue management provides immediate clinically relevant benefits without harmful effects for patients with nerve-related neck and arm pain: a randomised trial

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Om hvordan manipulering av vevet rundt nerver gir en umiddelbar bedring av nakkesmerter med utstårling ut armen.

http://ajp.physiotherapy.asn.au/AJP/vol_58/1/Nee.pdf

These results enable physiotherapists to inform patients that neural tissue management provides immediate clinically relevant benefits beyond advice to remain active with no evidence of harmful effects.

One month prevalence rates for activity-limiting neck pain range from 7.5% to 14.5% in the general population (Hogg-Johnson et al 2008, Webb et al 2003). Neck pain spreading down the arm is more common than neck pain alone and is associated with higher levels of self-reported disability (Daffner et al 2003). One mechanism for neck pain spreading down the arm is the sensitisation of neural tissues (Bogduk 2009).

Neural tissue management was based on principles proposed by Elvey (1986) and Butler (2000). Along with advice to continue their usual activities, participants assigned to the experimental group received an educational component, manual therapy techniques, and a home program of nerve gliding exercises. The educational component attempted to reduce unnecessary apprehension participants may have had about neural tissue management (Butler 2000). The manual therapy techniques and nerve gliding exercises have been advocated for reducing nerve mechanosensitivity (Butler 2000, Coppieters and Butler 2008, Elvey 1986).

The educational component emphasised two points. First, examination findings suggested that participants’ symptoms were at least partly related to nerves in the neck and arm that had become overly sensitive to movement. Second, neural tissue management techniques would move the nerves in a gentle and pain-free manner, aiming to reduce this sensitivity. The manual therapy techniques included a contralateral cervical lateral glide and a shoulder girdle oscillation combined with active craniocervical flexion to elongate the posterior cervical spine (Elvey 1986). The home program of nerve gliding exercises involved a ‘sliding’ and a ‘tensioning’ technique for the median nerve and cervical nerve roots (Coppieters and Butler 2008).

There was no evidence to suggest that neural tissue management was harmful. ‘Worst case’ intention-to- treat and ‘complete case’ analyses showed no difference in the prevalence of worsening between groups (Table 2).

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A novel protocol to develop a prediction model that identifies patients with nerve-related neck and arm pain who benefit from the early introduction of neural tissue management

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Om hvordan mobilisering av vevet rundt nervetrådene gir solid bedring på nakkesmerter med utstrålinger ut i armen. Studien har detaljert beskrivelse av teknikkene. Kan det være at den fikk så stor bedring ved at kriteriene ble satt på subjektiv opplevelse av «moderat bedring» av klientene?

http://www.sciencedirect.com/science/article/pii/S1551714411001455

We describe a novel protocol to develop a prediction model that identifies patients with nerve-related neck and arm pain who are likely to benefit from the early introduction of neural tissue management (NTM).

Patients rating themselves at least ‘moderately better’ on a Global Rating of Change scale will be considered ‘improved’.