When pain is not only pain: Inserting needles into the body evokes distinct reward-related brain responses in the context of a treatment.

Denne beskriver hvordan smerte ikke alltid er smerte, at konteksten smerte gis i bestemmer hvordan det oppleves. Forklart med dry needling, så vil nåle-smerten være mindre smertefullt og oppleves positivt om det blir gitt i en kontekst som oppleves postivit vet at det er en del av behandlingsopplegget for å bli smertefri.



The aim of this study was to compare behavioral and functional brain responses to the act of inserting needles into the body in two different contexts, treatment and stimulation, and to determine whether the behavioral and functional brain responses to a subsequent pain stimulus were also context dependent. Twenty-four participants were randomly divided into two groups: an acupuncture treatment (AT) group and an acupuncture stimulation (AS) group. Each participant received three different types of stimuli, consisting of tactile, acupuncture, and pain stimuli, and was given behavioral assessments during fMRI scanning. Although the applied stimuli were physically identical in both groups, the verbal instructions differed: participants in the AS group were primed to consider the acupuncture as a painful stimulus, whereas the participants in the AT group were told that the acupuncture was part of therapeutic treatment. Acupuncture yielded greater brain activation in reward-related brain areas (ventral striatum) of the brain in the AT group when compared to the AS group. Brain activation in response to pain stimuli was significantly attenuated in the bilateral secondary somatosensory cortex and the right dorsolateral prefrontal cortex after prior acupuncture needle stimulation in the AT group but not in the AS group. Inserting needles into the body in the context of treatment activated reward circuitries in the brain and modulated pain responses in the pain matrix. Our findings suggest that pain induced by therapeutic tools in the context of a treatment is modulated differently in the brain, demonstrating the power of context in medical practice.

The trigger point strikes … out!

En blog av Quinter som bedre forklarer det nevrologiske utgangspunktet for triggerpunkter, eller mer korrekt: ømme punkter og stramme muskler.

Basert på deres nye forklaringsmodell vil et problem (f.eks. betennelse) lenger inn på en sensorisk nerve sender betennelse (nevrogen betennelse) ut til muskelen, i tillegg til at motoriske og sympatiske (stress) signaler fra ryggmargen sendes ut til muskelen og gir en muskelspenning og twitchrespons vi kan se og kjenne med fingrene.

Ang. nevrogen betennelse så nevner wikipedia en studie på mus som viser at magnesium mangel, selv det som er innenfor «normalen» kan bidra til økt utskillelse av SP, som er en nevrogen betennelsesfaktor. http://en.wikipedia.org/wiki/Neurogenic_inflammation


But when I met the late Bob Elvey, he completely changed my way of thinking about these clinical problems. Bob’s mantra was that “muscles protect nerves.” He introduced me to the dynamics of the nervous system and I came to understand that peripheral nerves of the upper limb had evolved to be able to adapt to the various changes in limb position and length and that they were vulnerable at certain anatomical points along their course.


In brief, Geoff’s studies have had two major impacts on how we think about pain felt in muscles or other deep structures.

Firstly, he confirmed the presence of nociceptors with multiple receptive fields that branch within the nerve sheaths and extend to other deep tissues (nervi nervorum) [7]. The implication of this finding is that activity in a receptor in one structure such as the nerve sheath, could be perceived in another, such as the muscle.

Secondly, he showed that inflammation of nerves has profound effects on these same axons, the nociceptors to deep structures. These effects include ongoing activity and abnormal mechanical sensitivity [8, and others]. The implication of this finding is that this activity will be perceived by the brain in the area of the receptive fields mapped for the deep structure nociceptors, not in the area of the problem.


Figure 1. Proposed hypothesis for the development of focal muscle sensitivity and possible alteration in muscle texture with a proximal neural cause. Inflammation affecting a peripheral nerve (red spot) results in spontaneous and mechanically evoked afferent and efferent action potentials in small caliber sensory neurons innervating non-cutaneous structures, and decreased sympathetic discharge (-). These processes may cause reflex motor discharge sufficient to cause a palpable contraction (?), which combined with clinical phenomena associated with neurogenic inflammation (+), could explain the clinical phenomenon that has become known as a “trigger point.”


Diagnosis and management of adhesive capsulitis

Nevner det meste av medisinske behandlingsmetoder for frozen shoulder. Men kun medisiner eller kirurgi nevnes. Bedring fra 92% til 165% fremad elevasjon stående, og fra 12% til 52% utrotasjon av armen ryggliggende er resultatene av kirurgi. Dette har jeg også fått til ved hjelp av dry needling og behandlingene på Verkstedet.


Adhesive capsulitis is diagnosed by numerous physical characteristics including a thickening of the synovial capsule, adhesions within the subacromial or subdeltoid bursa, adhesions to the biceps tendon, and/or obliteration of the axillary fold secondary to adhesions [19].

Adhesive capsulitis has an incidence of 3–5% in the general population and up to 20% in those with diabetes. This disorder is one of the most common musculoskeletal problems seen in orthopedics [1115]. Although some have described adhesive capsulitis as a self-limiting disorder that resolves in 1–3 years [131620], other studies report ranges of between 20 and 50% of patients with adhesive caspulitis which suffer long-term ROM deficits that may last up to 10 years [2125].

Adhesive capsulitis is commonly associated with other systemic and nonsystemic conditions. By far the most common is the co-morbid condition of diabetes mellitus, with an incidence of 10–36% [142728].

Other co-morbid conditions include hyperthyroidism, hypothyroidism, hypoadrenalism, Parkinson’s disease, cardiac disease, pulmonary disease, stroke, and even surgical procedures that do not affect the shoulder such as cardiac surgery, cardiac catheterization, neurosurgery, and radical neck dissection [2939].

Adhesive capsulitis is classified into two categories: (1) primary, which is insidious and idiopathic, or (2) secondary, which is generally due to trauma or subsequent immobilization [41]. Those with primary adhesive capsulitis generally have a very gradual onset and progression of symptoms, with no known precipitating event that can be identified [42].

Adhesive capsulitis presentation is generally broken into three distinct stages [43]. The first stage that is described is called the freezing or painful stage. Patients may not present during this stage because they think that eventually the pain will resolve if self-treated.

This phase typically lasts between 3 and 9 months and is characterized by an acute synovitis of the glenohumeral joint [44].

Most patients will progress to the second stage, the frozen or transitional stage. During this stage shoulder pain does not necessarily worsen. Because of pain at end ROM, use of the arm may be limited causing muscular disuse. The frozen stage lasts anywhere 4 to 12 months [44].

The third stage begins when ROM begins to improve. This 3rd stage is termed the thawing stage. This stage lasts anywhere from 12 to 42 months and is defined by a gradual return of shoulder mobility.

Pain associated with adhesive capsulitis can cause a limitation or selective immobilization of the painful shoulder. Prolonged immobilization of a joint has been shown to cause several detrimental pathophysiologic findings including: decreased collagen length, fibrofatty infiltration into the capsular recess, ligament atrophy resulting in decreased stress absorption, collagen band bridging across recesses, random collagen production, and altered sarcomere number in muscle tissue [45].

Testing for impingement may be positive with a Hawkin’s or Neer sign; however, the pain is likely from the intrinsic process of impingement or capsular stretch rather than from adhesive capsulitis.

The diagnosis of adhesive capsulitis is often one of exclusion. Early in the disease process adhesive capsulitis may clinically appear similar to other shoulder conditions such as major trauma, rotator cuff tear, rotator cuff contusion, labral tear, bone contusion, subacromial bursitis, cervical or peripheral neuropathy. Additionally, a history of a previous surgical procedure can lead to shoulder stiffness. If a history of these other pathologies are negative and if radiographs do not demonstrate osteoarthritis, then the diagnosis can be given.

Non-operative treatment


Treatment of adhesive capsulitis often involves the use of anti-inflammatories, or corticosteroids. NSAIDs may be used during any phase as an attempt to relieve symptoms. There are no well done studies to indicate that NSAIDs change the natural history of adhesive capsulitis.

Intra-articular corticosteroid injections

Although high-quality randomized studies of corticosteroid injection for treatment of adhesive capsulitis have not been done, there is some evidence to indicate there is a short-term benefit with their use.

Surgical treatment

The treatment of adhesive capsulitis should lead to the operating room only after a concerted effort at conservative management has failed.

Manipulation under anesthesia

Manipulation under anesthesia as a means of treatment has been advocated. This method allows return of ROM in the operating room. Immediate postoperative physical therapy can be initiated with this form of treatment [49]. Manipulation under anesthesia has the disadvantage in that tissues that are stretched while the patient is under anesthesia may cause pain when awake. This can potentially slow recovery. When surgical release is added to this procedure it induces further surgical trauma to the shoulder and may slow rehabilitation.

Arthroscopic release and repair

Arthroscopy is an excellent additional tool for addressing the shoulder with adhesive capsulitis, and has become well accepted in treating this process. The essential lesion is the tightened coracohumeral ligament and rotator interval with the contracted capsule including the axillary pouch. These structures can be treated by release with arthroscopic instruments.

Operative treatment of adhesive capsulitis has been shown to decrease the duration of the disease and to return ROM with good success. Total recovery of pain-free ROM averages 2.8 months (1–6), and time for formal physical therapy averages 2.3 months (2–20) weeks. Forward elevation improved from the average of 92–165° and external rotation with the elbow at the side improved from 12 to 56° in a series of 68 shoulders treated with arthroscopic capsular release [61].

Patient education

Because adhesive capsulitis is so painful and has a very slow progression of resolution, patient education is critical for success. Patients should be educated in the chronicity of this condition. If they know and understand ahead of time that it can be several years before symptoms are completely resolved, apprehension and a feeling of urgency for functional return may be decreased.

Trigger point dry needling as an adjunct treatment for a patient with adhesive capsulitis of the shoulder.

Nevner at dry needling gir en raskere smertereduksjon og bevegelsesøkning ved frozen shoulder. 10 behandlinger ble gjort i dette tilfelle.




Prognosis for adhesive capsulitis has been described as self-limiting and can persist for 1 to 3 years. Conservative treatment that includes physical therapy is commonly advised.


The patient was a 54-year-old woman with primary symptoms of shoulder pain and loss of motion consistent with adhesive capsulitis. Manual physical therapy intervention initially consisted of joint mobilizations of the shoulder region and thrust manipulation of the cervicothoracic region. Although manual techniques seemed to result in some early functional improvement, continued progression was limited by pain. Subsequent examination identified trigger points in the upper trapezius, levator scapula, deltoid, and infraspinatus muscles, which were treated with dry needling to decrease pain and allow for higher grades of manual intervention.


The patient was treated for a total of 13 visits over a 6-week period. After trigger point dry needling was introduced on the third visit, improvements in pain-free shoulder range of motion and functional outcome measures, assessed with the Shoulder Pain and Disability Index and the shortened form of the Disabilities of the Arm, Shoulder and Hand questionnaire, exceeded the minimal clinically important difference after 2 treatment sessions. At discharge, the patient had achieved significant improvements inshoulder range of motion in all planes, and outcome measures were significantly improved.


This case report describes the clinical reasoning behind the use of trigger point dry needlingin the treatment of a patient with adhesive capsulitis. The rapid improvement seen in this patient following the initiation of dry needling to the upper trapezius, levator scapula, deltoid, and infraspinatus muscles suggests that surrounding muscles may be a significant source of pain in this condition.