Osteopathy-Physiotherapy Luang Prabang

27/07/2025

👉Phasen der Sehnenheilung ❗

Die biologische Kaskade, die die Sehnenheilung reguliert, gliedert sich in überlappende Phasen, die jeweils von unterschiedlichen Zelltypen gesteuert werden.

👉Jetzt auf physiomeets.science lesen! 🥳💪

13/07/2025

Just published 🔥

Infographic: Adhesive Capsulitis of the Shoulder

📘https://www.arthroscopyjournal.org/article/S0749-8063(25)00224-5/fulltext

▶️ Definition: Adhesive capsulitis is characterized by limited range of motion (ROM, https://pubmed.ncbi.nlm.nih.gov/30811157/) , as well as associated signs and symptoms including sleep disturbance, anxiety, and impaired functions that may impose a serious burden on patients’ activities of daily living (https://pubmed.ncbi.nlm.nih.gov/24078753/).

🔬 Pathophysiology: An inflammatory reaction progresses to fibrotic contracture, with active fibroblastic proliferation and collagen formation resulting in a stiff and thickened glenohumeral capsule with abundance of type III collagen. (https://pubmed.ncbi.nlm.nih.gov/33205235/)

🥶 Clinical Phases: The condition is classified into freezing, frozen, and thawing phases. However, owing to considerable overlap between stages, there is highly variable reference to the distinct stages in the literature presented, and its use in guidelines for treatment decision-making is limited (https://pubmed.ncbi.nlm.nih.gov/40291049/).

⚠️ Risk Factors: Diabetes, hyperthyroidism, prior fractures, shoulder or cervical spine surgery, and radiation therapy increase risk (https://www.ncbi.nlm.nih.gov/books/NBK532955/).

👩 Prevalence: Affects 2–5% of individuals, with higher rates in women. (https://pubmed.ncbi.nlm.nih.gov/21167743/)

🩺 Diagnosis: Plain radiographs are often unremarkable; Normal X-rays in two planes may be used to rule out mechanical glenohumeral incongruity such as arthritis, avascular necrosis or tumor, which might produce a similar clinical picture (https://pmc.ncbi.nlm.nih.gov/articles/PMC12018368/). MRI may show thickened capsule, synovial hypertrophy, and joint capsule edema.

💪 Nonsurgical Treatment: Focuses on pain relief and restoring ROM via physical therapy, oral anti-inflammatories, corticosteroid injections, extracorporeal shock wave therapy, and ultrasound-guided hydrodistention. (https://pubmed.ncbi.nlm.nih.gov/33292924/)

💉 Corticosteroid Injections: Early injections shorten symptom duration; rotator interval approach (https://pubmed.ncbi.nlm.nih.gov/29268022/) and lower doses (20 mg, https://pubmed.ncbi.nlm.nih.gov/37774178/) may yield better outcomes.

🌊 Hydrodilatation: Ultrasound-guided hydrodilatation with hyaluronic acid plus physical therapy shows superior results compared to physical therapy alone up to 12 weeks follow-up. (https://pubmed.ncbi.nlm.nih.gov/37697666/)

⚡️Diabetes Patients: Extracorporeal shock wave therapy avoids metabolic complications from steroids. (https://pubmed.ncbi.nlm.nih.gov/27899492/)

📊 Self-Limiting: Most patients achieve symptom improvement without surgery. But: The long-held theory of recovery phases leading to complete resolution without treatment for frozen shoulder is unfounded (https://pubmed.ncbi.nlm.nih.gov/30952550/).

🔧 Surgical Options: Considered after 9–12 months of failed nonsurgical management, including arthroscopic capsular release, manipulation under anesthesia (MUA), or both. (https://pmc.ncbi.nlm.nih.gov/articles/PMC11216839/)

👀 MUA vs. Arthroscopy: MUA is more cost-effective (https://pubmed.ncbi.nlm.nih.gov/36048234/) and arthroscopy had a higher risk of complications and adverse events during short term follow-up (https://pmc.ncbi.nlm.nih.gov/articles/PMC11216839/).

25/05/2025

02/03/2025

01/01/2025

🎊🌲Between the years, we traditionally announce our "Best-of series" of the most influential posts of 2024 on FB.

📣 today 🥇 10

💡Sciatic nerve innervation

👉 The sciatic nerve is the largest nerve in the body. It arises from the fourth and fifth lumbar and first three sacral nerve roots, which join in the lumbosacral plexus to form the fibular and tibial nerves (s. Figure).

👉 These leave the pelvis through the greater sciatic foramen, ensheathed as a single trunk, travelling distally in the posterior compartment of the thigh.

👉 The sciatic nerve provides sensory innervation to the skin of the foot and leg, and motor innervation to the posterior compartment of the thigh and all the compartments of the leg.

📷 Illustration: https://doi.org/10.12968/hmed.2016.77.11.C180

29/09/2024

Nociceptive and Neuropathic drivers of Neck Pain 💡

📘 Cohen & Hooten (2017), https://pubmed.ncbi.nlm.nih.gov/28807894/

👉 Facet Joints

On the basis of medial branch (facet joint nerve) blocks, the prevalence of cervical facet joint pain is estimated at 40-55% in patients with neck pain with or without whiplash (https://pubmed.ncbi.nlm.nih.gov/23159977/). However, without a standard for comparison, the accuracy of cervical facet blocks cannot be known, and their utility is controversial. Furthermore, diagnostic blocks are liable to false-positive responses and studies lack randomized, placebo-controlled blocks limiting their credability (https://pubmed.ncbi.nlm.nih.gov/26995797/).

👉 Cervical discogenic pain

Degenerated discs contain high levels of pro-inflammatory mediators (https://pubmed.ncbi.nlm.nih.gov/24753325/). More than 70% of people without neck pain have clinically significant disc degeneration by their mid-40s, (https://pubmed.ncbi.nlm.nih.gov/19333104/) with the prevalence rising above 85% by age (https://pubmed.ncbi.nlm.nih.gov/9460946/). Disc degeneration also increases the likelihood of herniation (https://pubmed.ncbi.nlm.nih.gov/10949442/). The high prevalence of neck pain and disc abnormalities in asymptomatic people provides the conceptual appeal for discography, which is advocated as the only test that connects disease to symptoms. A systematic review evaluating the accuracy of cervical discography found prevalence rates of 16-53% (https://pubmed.ncbi.nlm.nih.gov/23159976/). But discography is an invasive procedure that carries a small risk of catastrophic consequences and a high false positive rate in certain populations (https://pubmed.ncbi.nlm.nih.gov/14133649/).

👉 Cervical Disk Herniation

The annual incidence of cervical radiculopathy resulting from disc protrusion or degenerative spondylosis (or both) is estimated at 1-3.5 per 1000 person years, peaking in the sixth decade of life (https://pubmed.ncbi.nlm.nih.gov/8186959/, https://pubmed.ncbi.nlm.nih.gov/21430568/). The most commonly affected levels are C7 (45-60%), C6 (20-25%), and C5 and C8 (10%) (https://pubmed.ncbi.nlm.nih.gov/25659245/, https://pubmed.ncbi.nlm.nih.gov/8186959/). Not all radicular symptoms result from mechanical nerve root compression. Similar to the lumbar spine, cytokines and other inflammatory mediators play a pivotal role in cervical radicular pain (https://pubmed.ncbi.nlm.nih.gov/24166242/, https://pubmed.ncbi.nlm.nih.gov/20309734/). Furthermore, not all disc herniations are painful: Studies in asymptomatic volunteers report the prevalence of disc herniation as 2-23%, with a median of 11% (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3611065/, https://pubmed.ncbi.nlm.nih.gov/9460946/).

👉 Cervical spinal stenosis

Spinal stenosis can be classified as central, involving the lateral recesses, or foraminal, with the last two types generally affecting the exiting nerve root(s). The incidence of symptomatic central cervical spinal stenosis, in which the spinal canal diameter measures less than 10 mm, is estimated to be one in 100 000 but significantly increases over the age of 50 years (https://pubmed.ncbi.nlm.nih.gov/24365318/). Spinal stenosis has many causes, which can broadly be categorized as congenital (for example, short pedicles), spondylotic (for example, degenerative discs, hypertrophied facet joints and ligaments, and osteophytes), iatrogenic (for example, surgery), traumatic, metabolic (for example, Paget’s disease), and rheumatologic (for example, spondyloarthropathy).

👉 Atlanto-axial (AA) and Atlanto-occipital (AO) Joints

Pain arising from C1–C2 most often occurs in the suboccipital region, commonly extending cephalad into the head or caudad into the upper neck. Referred pain patterns have been studied in healthy volunteers without neck pain as well as in those with proven cervical joint pain (https://pubmed.ncbi.nlm.nih.gov/17610457/, https://pubmed.ncbi.nlm.nih.gov/8059267/, https://pubmed.ncbi.nlm.nih.gov/9252002/). AO-mediated pain has consistently been reported as suboccipital, but may extend to the frontal area, slightly anterior to the vertex (https://pubmed.ncbi.nlm.nih.gov/8059267/).

👉 Cervicogenic Headache

A cervicogenic headache is thought to be referred pain arising from irritation caused by cervical structures innervated by spinal nerves C1, C2, and C3; therefore, any structure innervated by the C1–C3 spinal nerves could be the source of a cervicogenic headache (https://pubmed.ncbi.nlm.nih.gov/19747657/). The best available studies indicate that the C2–3 zygapophysial joints are the most common source of cervicogenic headache, https://pubmed.ncbi.nlm.nih.gov/17610457/, https://pubmed.ncbi.nlm.nih.gov/7931379/, https://pubmed.ncbi.nlm.nih.gov/3175750/, accounting for about 70% of cases. (https://pubmed.ncbi.nlm.nih.gov/2402682/)

👉 Myofascial pain

Myofascial pain is a common cause of neck pain that involves discrete or diffuse areas of sensitivity within one or more muscle. The causes of myofascial pain are poorly understood, but muscle pain can develop secondary to biomechanical imbalances, trauma, emotional stress, and even endocrine and hormonal abnormalities. Tender muscles release excess acetylcholine, which can result in dysfunctional motor endplates, sustained muscle contractions, local ischemia, sarcomere shortening, and the release of inflammatory mediators, in what can devolve into a vicious circle (https://pubmed.ncbi.nlm.nih.gov/19728962/).

24/09/2024

Inflammatory mechanisms as a potential cause of radicular pain in lumbar disc herniation (LDH)

👫 Lumbar disc herniation (LDH), a condition resulting from the protrusion of the intervertebral disc material into the spinal canal, is a prevalent cause of low back pain and radicular pain known as sciatica. (https://pubmed.ncbi.nlm.nih.gov/25806916/)

🗜️ The precise mechanisms underlying sciatica in LDH remain incompletely understood. Historically, the pathogenesis of sciatica was attributed to mechanical compression of the nerve roots. However, human studies have unequivocally shown that compression of healthy nerve roots typically leads to paresthesia and numbness, rather than the sensation of pain (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900171/).

🔥 Animal-based research has revealed that compression of a healthy nerve root triggers a transient discharge, which is fleeting in nature and insufficient to explain the occurrence of radicular pain. Additionally, numerous patients who are diagnosed with lumbar radicular pain solely based on clinical assessment do not exhibit any signs of nerve root disease in imaging evaluations (https://pubmed.ncbi.nlm.nih.gov/17704089/). These studies suggest that factors beyond mere nerve compression, such as inflammation, contribute to the perception of pain in LDH.

📘 A brand-new paper by Zhou et al. hypothesizes that inflammatory mechanisms, particularly the release of cytokines like interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α), from the herniated disc material, initiate and sustain local inflammation. (https://www.sciencedirect.com/science/article/pii/S0306987724002287)

🔥 It is postulated that the herniation of intervertebral disc tissue into the epidural space triggers a foreign-body reaction, characterized by macrophage infiltration (https://pubmed.ncbi.nlm.nih.gov/24635921/). These macrophages play a crucial role in inducing an inflammatory response, potentially leading to the experience of pain. In patients with lumbar disc herniation experiencing sciatica or low back pain, elevated levels of inflammatory cytokines, including IL-1a, IL-1b, IL-6, IL-8, TNF-α, and prostaglandin E2, have been detected in discectomy specimens, indicating an inflammatory etiology underlying radicular pain (https://pubmed.ncbi.nlm.nih.gov/11924650/).

👉IL-6: Acts as an inflammatory mediator and enhances pain sensitivity by activating nociceptors.
👉IL-8: Attracts immune cells (like neutrophils) to the site of inflammation, exacerbating the response and contributing to pain.
👉TNF-α: A major initiator of inflammation, which directly activates nociceptors and induces the release of other cytokines, perpetuating a cycle of inflammation and pain.

🔼 This inflammatory response can persist independently of mechanical compression and continues even after herniation reduces. These cytokines sensitize nociceptors, leading to heightened pain perception and neuropathic pain. Once sensitized, these nociceptors become hyperresponsive to mechanical compression.

💡 If inflammatory mechanisms are indeed primarily involved in the genesis of sciatica, this would suggest that pharmacological and non-pharmacological anti-inflammatory therapies (i.e. exercise therapy, https://pubmed.ncbi.nlm.nih.gov/36690283/, https://pubmed.ncbi.nlm.nih.gov/39144705/ or neural mobilization, https://pubmed.ncbi.nlm.nih.gov/25892373/) may be beneficial in treating this condition.

29/12/2023

Just published in Pain Practice 🔥

Sacroiliac joint pain
https://pubmed.ncbi.nlm.nih.gov/38155419/

💡 Physical examination🤚

👉 "Although solitary pain provocation maneuvers have no pathognomonic value in identifying a painful SI joint, two individual pain provocation tests- the compression and thigh thrust test- may be helpful in diagnosing SI joint pain. https://pubmed.ncbi.nlm.nih.gov/19101212/

👉 Patients with a positive thigh thrust test or compression test may be more likely to suffer from intra-articular SI joint pain [sensitivity 0.907 (0.78–0.97), specificity 0.662 (0.53–0.77), diagnostic odds ratio 18.461 (5.82–58.53)]. Due to the size and the immobility of the SI interface, large forces are needed to stress the joint, which can be a source of false negatives.

👉 In addition, if forces are applied incorrectly, pain can be provoked in neighboring structures, resulting in false-positive tests. Both the sensitivity and specificity of the clinical examination increases as a direct function of the number of positive tests. Two studies found that three or more positive provocative tests resulted in a specificity and sensitivity of 79% and 85%, and 78% and 94%, respectively. https://pubmed.ncbi.nlm.nih.gov/16401431/, https://pubmed.ncbi.nlm.nih.gov/16038856/

👉 This was confirmed by a meta-analysis which showed that 3 or more positive stress tests have discriminative power for diagnosing SI joint pain. https://pubmed.ncbi.nlm.nih.gov/19101212/

📊 However, three recent studies call into question the diagnostic value of individual or a battery of provocative tests. https://pubmed.ncbi.nlm.nih.gov/31393577/, https://pubmed.ncbi.nlm.nih.gov/32965780/, https://pubmed.ncbi.nlm.nih.gov/34880117/

📈 In a systematic review involving five studies and 422 patients, Saueressig et al. (Physio Meets Science) found that a battery of positive provocative SI joint maneuvers had only a 35% certainty of identifying the SI joint as the primary pain generator, but that a negative cluster of tests is associated with a non-painful joint in 92% of cases." https://pubmed.ncbi.nlm.nih.gov/34210160/

Figure: Typical pain referral pattern of sacroiliac joint pain

14/06/2023

Just published in British Journal of Sports Medicine (BJSM)🔥

Healing of acute anterior cruciate ligament rupture on MRI and outcomes following non-surgical management with the Cross Bracing Protocol

https://bjsm.bmj.com/content/early/2023/06/13/bjsports-2023-106931

😲"After management of acute ACL rupture with the Cross Bracing Protocol (CBP), that aims to reduce the gap distance between the ligament remnants by immobilising the knee at 90° of flexion for 4 weeks in an attempt to facilitate bridging of tissue and healing between the ruptured ACL remnants., 90% of patients had evidence of healing on 3-month MRI (continuity of the ACL).

😲 More ACL healing on 3-month MRI was associated with better outcomes. Longer-term follow-up and clinical trials are needed to inform clinical practice."

08/05/2023

Exercise for rotator cuff tendinopathy: Proposed mechanisms of recovery 💡

https://journals.sagepub.com/doi/10.1177/17585732231172166

👉 Rotator cuff (RC) tendinopathy is a common cause of musculoskeletal shoulder pain. (https://pubmed.ncbi.nlm.nih.gov/15769790/, https://pubmed.ncbi.nlm.nih.gov/21936616/)

👉 The prevalence in the general population ranges from 2.4% to 14%3 and it can go up to 45% in manual repetitive workers. (https://pubmed.ncbi.nlm.nih.gov/14691271/)

👉 Recovery of RC tendinopathy is limited, with 40%–50% of patients developing recurrent chronic symptoms. (https://pubmed.ncbi.nlm.nih.gov/25103016/, https://pubmed.ncbi.nlm.nih.gov/36300352/)

👉 Physical therapy is the first-line treatment for RC tendinopathy. Specifically, resisted exercise is the first-line recommended intervention in clinical practice guidelines. (https://pubmed.ncbi.nlm.nih.gov/32007452/, https://pubmed.ncbi.nlm.nih.gov/35881707/)

📍 In a brand-new review, Vila-Dieguez and colleagues proposed 4 mechanistic domains of factors forresisted exercise in patients with RC tendinopathy: tendon structure, neuromuscular, pain and sensorimotor processing, and psychosocial. The proposed four domains are based on the current evidence of both deficits in patients with RC tendinopathy and the impact of resisted exercise on these specific factors. (https://journals.sagepub.com/doi/10.1177/17585732231172166)

1⃣ Tendon structure: Tendon structure is complex; characterized by morphology (tendon thickness, https://pubmed.ncbi.nlm.nih.gov/34656782/, tendon collagen organization, https://pubmed.ncbi.nlm.nih.gov/28502699/), mechanical properties, material properties (i.e. decreased tendon stiffness https://pubmed.ncbi.nlm.nih.gov/30120723/ https://pubmed.ncbi.nlm.nih.gov/30689398/) , vascularity (neovascularization, https://pubmed.ncbi.nlm.nih.gov/20025761/, https://pubmed.ncbi.nlm.nih.gov/28081996/) and genetics. (https://pubmed.ncbi.nlm.nih.gov/28619548/) Patients with RC tendinopathy often have changes to multiple aspects of tendon structure. (https://pubmed.ncbi.nlm.nih.gov/28619548/, https://pubmed.ncbi.nlm.nih.gov/33396219/, https://pubmed.ncbi.nlm.nih.gov/15679569/)

2⃣ Neuromuscular factors: Mechanistic models of RC tendinopathy propose that repetitive motion overloads the tendon, leading to degeneration, which is associated with neuromuscular deficits. (https://pubmed.ncbi.nlm.nih.gov/20846766/, https://pubmed.ncbi.nlm.nih.gov/33414454/, https://pubmed.ncbi.nlm.nih.gov/27127294/).

Kinematic changes in scapulothoracic, scapulohumeral, sternoclavicular, and acromioclavi-cular joints (i.e. decreased upward rotation and posterior tilt in the scapulothoracic joint, https://pubmed.ncbi.nlm.nih.gov/25103135/, https://pubmed.ncbi.nlm.nih.gov/22388171/) have traditionally been discussed in the context of the extrinsic shoulder impingement theory. (https://pubmed.ncbi.nlm.nih.gov/23572144/). Maladaptive muscle activation pattern (i.e. delay of the lower trapezius in shoulder elevation, https://pubmed.ncbi.nlm.nih.gov/24389333/, https://pubmed.ncbi.nlm.nih.gov/28405223/) and reduced forced production or rate of force development (RFD, https://journals.lww.com/acsm-msse/Fulltext/2022/09002/Increased_Rate_Of_Force_Development_Is_Correlated.1785.aspx) are therapeutic targets in motor control and strength focussed rotator cuff exercise programs. https://pubmed.ncbi.nlm.nih.gov/36796859/

3⃣ Psychosocial factors: Psychological factors are associated with poor clinical outcomes in patients with musculoskeletal shoulder pain, (https://pubmed.ncbi.nlm.nih.gov/27445360/, https://pubmed.ncbi.nlm.nih.gov/30791696/) and specifically those with RC tendinopathy (https://pubmed.ncbi.nlm.nih.gov/32452391/). These psychological factors include depression, anxiety, sleep disturbance, distress, pain catastrophizing, kinesiophobia, self-efficacy, expectations of recovery, and resilience. (https://pubmed.ncbi.nlm.nih.gov/29654040/, https://pubmed.ncbi.nlm.nih.gov/29980139/, https://pubmed.ncbi.nlm.nih.gov/26677233/, https://pubmed.ncbi.nlm.nih.gov/30791696/). The authors speculate that exercise may influence psychological health and/or be a mediator by which resisted exercise produces beneficial outcomes.

4⃣ Nociceptive and sensorimotor processing: Emerging evidence suggests central nervous system dysfunction exists in RC tendinopathy. Decreased corticospinal excitability (https://pubmed.ncbi.nlm.nih.gov/25043198/) and increased pain sensitivity (https://pubmed.ncbi.nlm.nih.gov/25739842/) are related to worse clinical outcomes. Cortical reorganization and improved cortical excitability have been demonstrated following exercise in other musculoskeletal conditions. (https://pubmed.ncbi.nlm.nih.gov/33383996/, https://pubmed.ncbi.nlm.nih.gov/20181504/). Exercise may improve sensorimotor excitability resulting in improved muscular activation and decrease central sensitization (https://pubmed.ncbi.nlm.nih.gov/25739842/) in RC tendinopathy.

📣 This framework provides clinicians with a mechanistic model of four unique constructs to consider how exercise can improve pain and disability. Resisted exercise may normalise these factors, but there is limited evidence to explain the relationship of the four proposed domains to the trajectory of recovery and the identification of persistent deficits that limit outcomes. The presence of each mechanistic construct may vary between patients and over time. Identifying baseline deficits and the change in deficits over the course of the exercise intervention may help to refine and deliver patient-specific exercise that can optimise patient outcomes, or use a stepped and tailored approach to refer to alternative care.

Illustration: Theoretical model of mechanisms of rotator cuff tendinopathy. The table contains the summary of the evidence for the mechanisms of exercise; evidence rate by Oxford Centre for Evidence-Based Medicine 2011 Levels of Evidence. (https://journals.sagepub.com/doi/10.1177/17585732231172166)