Centre de formation et physiothérapie de Lutry

25/02/2026

Podcast Episode · JOSPT Insights · February 23 · 24m

22/02/2026

𝗠𝘂𝘀𝗰𝗹𝗲 𝗵𝘆𝗽𝗲𝗿𝘁𝗿𝗼𝗽𝗵𝘆 𝗳𝗿𝗼𝗺 𝗽𝗮𝗿𝘁𝗶𝗮𝗹 𝗿𝗲𝗽𝗲𝘁𝗶𝘁𝗶𝗼𝗻 𝗮𝘁 𝗹𝗼𝗻𝗴 𝘃𝘀. 𝘀𝗵𝗼𝗿𝘁 𝗺𝘂𝘀𝗰𝗹𝗲 𝗹𝗲𝗻𝗴𝘁𝗵: 𝗔 𝘀𝘆𝘀𝘁𝗲𝗺𝗮𝘁𝗶𝗰 𝗿𝗲𝘃𝗶𝗲𝘄 𝗮𝗻𝗱 𝗺𝗲𝘁𝗮-𝗮𝗻𝗮𝗹𝘆𝘀𝗶𝘀

📘 A recent systematic review and meta-analysis by Strey and colleagues (https://link.springer.com/article/10.1007/s11332-025-01586-5) examined whether resistance training performed at longer muscle lengths (LL) leads to greater muscle hypertrophy than training performed at shorter muscle lengths (SL).

SL resistance training was defined as any angle interval from 0 to half of the Full ROM, LL as any interval from half of the Full ROM.

Eight randomized controlled trials involving a total of 138 participants met the inclusion criteria. Muscle size was assessed using MRI or ultrasound. All interventions lasted at least four weeks.

📋 The included studies investigated several muscle groups. Most data were available for the quadriceps, including the vastus lateralis (n = 5), re**us femoris (n = 3), vastus medialis (n = 2), and vastus intermedius (n = 2). Additional muscles examined included the medial and lateral gastrocnemius (n = 1 each), as well as the biceps brachii and brachialis (n = 1).

💪 Across studies, resistance training performed at longer muscle lengths resulted in significantly greater increases in muscle size compared with training at shorter muscle lengths (ES = 0.283; 95% CI 0.04–0.52; p = 0.036). Analyses of regional hypertrophy showed a similar pattern. Long-length training produced greater hypertrophy in the distal (ES = 0.433; 95% CI 0.01–0.85; p = 0.048) and central muscle regions (ES = 0.276; 95% CI 0.01–0.48; p = 0.028), whereas differences in proximal hypertrophy were less clear.

💡Several mechanisms may account for the advantage observed with training at longer muscle lengths. One explanation is the higher mechanical tension typically generated in lengthened positions. Increased passive and active tension may provide a stronger stimulus for muscle growth. In addition, stretch-related signaling pathways have been proposed as potential contributors, especially increased mTOR activity and greater satellite cell activation. At present, however, it remains difficult to distinguish the specific effects of muscle stretch from those of increased force production. Previous work by Kubo and colleagues (https://pubmed.ncbi.nlm.nih.gov/16643193) reported force levels approximately 2.3 times higher at longer muscle lengths, suggesting that mechanical tension alone could explain at least part of the observed hypertrophy differences. A review by Wolf and colleagues

𝗣𝗿𝗮𝗰𝘁𝗶𝗰𝗮𝗹 𝗜𝗺𝗽𝗹𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀 𝗳𝗼𝗿 𝗧𝗵𝗲𝗿𝗮𝗽𝗶𝘀𝘁𝘀

▶️ From a rehabilitation perspective, the findings suggest that resistance exercises performed in lengthened muscle positions offer a modest but consistent advantage for promoting muscle hypertrophy. Whenever symptoms allow, exercises should include loading at longer muscle lengths, such as deeper joint angles (i.e. squat, https://pubmed.ncbi.nlm.nih.gov/31230110/) or positions closer to end range.

▶️ When full range-of-motion training is not feasible, loading the lengthened portion of the range appears preferable to working primarily in shortened positions. This approach may help preserve or stimulate muscle growth even when joint motion is limited.

▶️ Because exercises performed at longer muscle lengths may initially produce greater mechanical stress and muscle soreness, a gradual progression toward end-range loading is advisable. Carefully staged increases in range of motion and intensity may improve tolerance while still taking advantage of the hypertrophic stimulus associated with lengthened training.

21/02/2026

"Strengthening interventions that include eccentric exercises and neuromuscular electrical stimulation may yield the most substantial improvements in shoulder abduction, external rotation, and internal rotation strength"

Our latest review and of shoulder interventions ➡️ https://ow.ly/XaYW50Yj95V

20/02/2026

𝗠𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺 𝗼𝗳 𝗔𝗰𝘁𝗶𝗼𝗻 𝗼𝗳 𝗧𝗵𝗲𝗿𝗮𝗽𝗲𝘂𝘁𝗶𝗰 𝗘𝘅𝗲𝗿𝗰𝗶𝘀𝗲 𝗶𝗻 𝗥𝗼𝘁𝗮𝘁𝗼𝗿 𝗖𝘂𝗳𝗳 𝗧𝗲𝗻𝗱𝗶𝗻𝗼𝗽𝗮𝘁𝗵𝘆: 𝗪𝗵𝗮𝘁 𝗗𝗼𝗲𝘀 𝗘𝗹𝗮𝘀𝘁𝗼𝗴𝗿𝗮𝗽𝗵𝘆 𝗔𝗱𝗱?

We prescribe strengthening exercises for rotator cuff–related shoulder pain almost automatically. They’re guideline-supported (https://pubmed.ncbi.nlm.nih.gov/40165544/, https://pubmed.ncbi.nlm.nih.gov/32007452/), widely used, and clinically effective. But what actually drives improvement?

📘 A brand-new study by Pérez-Porta and colleagues (https://pubmed.ncbi.nlm.nih.gov/41682699/) explored two potential mechanisms: strength gains and changes in supraspinatus muscle properties. Thirty-nine patients with rotator cuff–related shoulder pain (no full-thickness tears) completed a 6-month progressive strengthening program.

🏋️‍♂️ The program included (s. picture in comments):
Rotator cuff strengthening (especially abductors and external rotators)
Periscapular strengthening (protractors and retractors)
Posterior capsule stretching when indicated

Patients had five supervised sessions over three weeks, plus follow-ups at weeks 6 and 12 to progress loading. Exercises were progressed based on pain (≤4/10) or perceived exertion (≥6/10 if pain-free).

💪 Strength was measured with dynamometry. Supraspinatus muscle stiffness was assessed using shear wave elastography (SWE), which quantifies tissue stiffness via shear wave velocity.

📊 Results

✅ Clinically, most patients improved. Nearly 70% reported being much better or fully recovered.

✅ Strength gains, however, were small and not statistically significant. Even clearly improved patients did not show dramatic strength increases.

✅ What did change was muscle stiffness. After six months, supraspinatus stiffness at rest increased. Patients who improved functionally showed a clearer increase in resting stiffness than those who did not. Strength did not follow the same pattern.

✅ In this specific population — without major structural degeneration — increased stiffness is interpreted cautiously as a potential sign of improved muscle density or tissue quality rather than fibrosis. The authors suggest this may reflect adaptive remodeling in response to sustained loading.

💡 For practitioners, this is the interesting part: A well-structured, progressive strengthening program targeting cuff and scapular musculature may induce measurable changes in muscle properties — even if strength gains look modest. So perhaps exercise in RCRSP works less by dramatically increasing force output and more by gradually restoring tissue load capacity and muscle quality.

❎ Limitations: Small study. Exploratory data. Non-blinded assessor.

🤔 Maybe we’re not just building strength. Maybe we’re building better tissue. Further studies will show.

18/02/2026

A cross-sectional study of 602 Finnish adults found that abnormalities on magnetic resonance imaging ( ) were nearly universal after age 40, with 99% of participants displaying some abnormality.

The prevalence and severity of these abnormalities increased with age, but did not differ between sexes. Importantly, rotator cuff abnormalities were present in both asymptomatic (96%) and symptomatic (98%) shoulders, and only full-thickness tears were weakly associated with symptoms, suggesting most imaging findings reflect normal age-related changes.

https://ja.ma/4aE9URm

16/02/2026

Our October 2025 discussed why the labelling of what we currently know as Medial Tibial Stress Syndrome should change...

Moving from 'MTSS' to 'LIMP'

Read why 👉 https://ow.ly/QZWI50X6tuW

15/02/2026

🧠 𝗜𝘀 𝗜𝘁 𝗧𝗶𝗺𝗲 𝘁𝗼 𝗥𝗲𝘁𝗶𝗿𝗲 "𝗡𝗼𝗰𝗶𝗽𝗹𝗮𝘀𝘁𝗶𝗰 𝗣𝗮𝗶𝗻"? 𝗔 𝗣𝗿𝗼𝗽𝗼𝘀𝗮𝗹 𝗳𝗼𝗿 𝗮 𝗨𝗻𝗶𝗳𝗶𝗲𝗱 𝗡𝗲𝘂𝗿𝗼𝗽𝗮𝘁𝗵𝗶𝗰 𝗣𝗮𝗶𝗻 𝗙𝗿𝗮𝗺𝗲𝘄𝗼𝗿𝗸

■ A recent review published in Frontiers in Pain Research challenges the current international standards for pain classification.
■ Authored by Katsuhiro Toda, the paper argues that the introduction of "nociplastic pain" has created significant confusion in both clinical practice and academic research.
■ Toda proposes a controversial but pragmatic solution: integrate nociplastic pain back into the definition of neuropathic pain.

📚 𝗧𝗵𝗲 𝗖𝘂𝗿𝗿𝗲𝗻𝘁 𝗟𝗮𝗻𝗱𝘀𝗰𝗮𝗽𝗲

■ According to the International Association for the Study of Pain, pain is currently classified into three categories based on etiology.
■ Nociceptive Pain NcP: Pain from tissue damage.
■ Neuropathic Pain NeP: Pain caused by a lesion or disease of the somatosensory nervous system.
■ Nociplastic Pain NpP: Pain arising from altered nociception without clear evidence of tissue damage or a lesion to the somatosensory system adopted in 2017.
■ While this classification was intended to clarify diagnoses, Toda argues it has introduced "substantial uncertainty" and lacks clinical utility.

⚠️ 𝗧𝗵𝗲 𝗖𝗼𝗿𝗲 𝗣𝗿𝗼𝗯𝗹𝗲𝗺: 𝗗𝗶𝗮𝗴𝗻𝗼𝘀𝗶𝘀 𝗮𝗻𝗱 𝗔𝗺𝗯𝗶𝗴𝘂𝗶𝘁𝘆

■ The review highlights several critical gaps in the current NpP framework.
■ Lack of Evidence-Based Diagnosis:
■ There is currently no objective, evidence-based method to diagnose NpP.
■ The distinction often relies on the absence of a detectable lesion.
■ However, as diagnostic technology advances, lesions may be found in conditions currently labeled NpP.
■ The author draws a parallel to Parkinson’s disease, which was once thought to lack lesions before medical technology advanced.
■ Questionnaire Failure:
■ Most diagnostic questionnaires like painDETECT, DN4, and LANSS were developed before NpP was officially adopted in 2017.
■ Consequently, these tools cannot reliably distinguish between NeP and NpP.
■ In fact, they often classify NpP conditions as NeP.
■ The "Unified" vs. "Separate" NeP Confusion:
■ The author identifies a major academic ambiguity.
■ "NeP" is currently used to mean two different things.
■ Unified NeP: The older concept that included what we now call NpP.
■ Separate NeP: The new IASP definition that strictly excludes NpP.
■ Because researchers use these terms interchangeably without distinction, it is creating a "fragmented" evidence base.

🏥 𝗧𝗵𝗲 𝗖𝗹𝗶𝗻𝗶𝗰𝗮𝗹 𝗥𝗲𝗮𝗹𝗶𝘁𝘆: 𝗙𝗶𝗯𝗿𝗼𝗺𝘆𝗮𝗹𝗴𝗶𝗮 𝗮𝗻𝗱 𝗧𝗿𝗲𝗮𝘁𝗺𝗲𝗻𝘁

■ Toda uses Fibromyalgia FM—the prototypical nociplastic condition—to illustrate why the separation of NpP and NeP is flawed.
■ Diagnostic Overlap:
■ Research indicates that FM is frequently associated with small fiber neuropathy.
■ When patients with FM are assessed using standard questionnaires, at least half are identified as having Neuropathic Pain.
■ Therapeutic Redundancy:
■ From a treatment perspective, the distinction is almost meaningless.
■ The pharmacological treatments for NeP SNRIs, amitriptyline, gabapentinoids are the same treatments used for FM.
■ Similarly, non-pharmacological interventions like exercise and CBT are effective for both.
■ The Argument:
■ If the symptoms overlap, the underlying mechanisms central sensitization overlap, and the treatments are identical, why maintain two separate categories?

🧩 𝗧𝗵𝗲 𝗣𝗿𝗼𝗽𝗼𝘀𝗮𝗹: 𝗔 𝗥𝗲𝘃𝗶𝘀𝗲𝗱 𝗖𝗹𝗮𝘀𝘀𝗶𝗳𝗶𝗰𝗮𝘁𝗶𝗼𝗻

■ To resolve this confusion, the author proposes four provisional plans, with a strong recommendation for Plan 1.
■ The Recommended Plan:
■ Integrate Nociplastic Pain NpP into Neuropathic Pain NeP.
■ Under this proposal, clinicians would stop using the term NpP and classify these conditions as NeP.
■ This acknowledges that conditions like Fibromyalgia likely involve nervous system dysfunction, even if a specific lesion isn't visible on a standard MRI.
■ Alternative Proposals:
■ Subcategorization: Keep NpP but classify it as a subcategory of NeP.
■ New Terminology: Adopt the term "new NeP" nNeP to distinguish the integrated concept from previous definitions.

✅ 𝗕𝗲𝗻𝗲𝗳𝗶𝘁𝘀 𝗼𝗳 𝗜𝗻𝘁𝗲𝗴𝗿𝗮𝘁𝗶𝗼𝗻

■ Simplified Practice for Non-Specialists:
■ Most clinicians are not pain specialists.
■ Reducing the classification to two main types Nociceptive and Neuropathic simplifies decision-making.
■ Broadened Treatment Options:
■ Unifying the categories allows evidence from NeP treatments to be applied to NpP patients and vice versa, potentially improving patient care.
■ Reducing Stigma:
■ The ambiguity of NpP has sometimes led to it being conflated with "psychogenic pain."
■ Classifying these conditions as Neuropathic validates the biological basis of the patient's pain.
■ Aligning Science and Practice:
■ It bridges the gap between basic science which studies mechanisms and clinical practice which focuses on treatment outcomes.

📌 𝗖𝗼𝗻𝗰𝗹𝘂𝘀𝗶𝗼𝗻

■ The review concludes that while the introduction of Nociplastic Pain was well-intentioned, it currently creates more problems than it solves.
■ Until diagnostic tools can definitively distinguish NpP from NeP, Toda argues that NeP should be the unified term.
■ This change aims to resolve scholarly uncertainty, simplify clinical guidelines, and ultimately improve patient care.

-----------------
⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

15/02/2026

Relevant for differrentiation from T4 syndrome

Hot off the Press 🔥

𝗣𝗵𝘆𝘀𝗶𝗰𝗮𝗹 𝗮𝘀𝘀𝗲𝘀𝘀𝗺𝗲𝗻𝘁 𝗮𝗻𝗱 𝗿𝗲𝗵𝗮𝗯𝗶𝗹𝗶𝘁𝗮𝘁𝗶𝗼𝗻 𝗳𝗼𝗿 𝗻𝗲𝘂𝗿𝗼𝗴𝗲𝗻𝗶𝗰 𝘁𝗵𝗼𝗿𝗮𝗰𝗶𝗰 𝗼𝘂𝘁𝗹𝗲𝘁 𝘀𝘆𝗻𝗱𝗿𝗼𝗺𝗲 (𝗡𝗧𝗢𝗦): 𝗔 𝘀𝗰𝗼𝗽𝗶𝗻𝗴 𝗿𝗲𝘃𝗶𝗲𝘄

💁‍♂️ Neurogenic Thoracic Outlet Syndrome (NTOS) represents a significant clinical challenge within musculoskeletal and hand therapy, characterized by the dynamic compression of the brachial plexus. Neurogenic Thoracic Outlet Syndrome (NTOS) accounts for up to 95% of TOS csaes and is regarded as the more controversial and complex TOS subgroup due to the complexity of diagnosis and the constellation of signs and symptoms (https://pubmed.ncbi.nlm.nih.gov/36018621/, https://pubmed.ncbi.nlm.nih.gov/31037504/). NTOS is estimated to have a prevalence of 10 cases per 100,000 with an incidence of 2–3 cases per 100,000 per year (https://pubmed.ncbi.nlm.nih.gov/35978467/).

While specialist rehabilitation is widely considered the primary conservative treatment, the specific components of such programs have historically remained ill-defined and poorly reported. Early systematic reviews, such as the one conducted by Lo et al. (https://www.ncbi.nlm.nih.gov/books/NBK127550/) highlighted a lack of high-quality evidence regarding exercise efficacy, a sentiment echoed by the 2014 Cochrane review (https://pubmed.ncbi.nlm.nih.gov/25427003/) which noted the field was dominated by low-quality data. More recently, Luu et al. (https://pubmed.ncbi.nlm.nih.gov/35655698/) provided a scoping review of proposed exercise rationales, yet a detailed synthesis of comprehensive rehabilitation protocols and their clinical reasoning strategies was still lacking.

📘A brand-new scoping review by O'Sullivan et al. (https://pubmed.ncbi.nlm.nih.gov/41657761/) addressed this gap by analyzing 29 studies published since 2000 to map current physical assessment and rehabilitation practices. The findings reveal that assessment is heavily weighted toward diagnostic confirmation rather than identifying specific therapeutic targets. The most prevalent tools include provocation tests—specifically the Elevated Arm Stress Test (EAST), Upper Limb Tension Test (ULTT), and Adson’s test—alongside palpation of the pectoralis minor, scalenes, scalene triangle, subcoracoid space. Postural and scapulothoracic assessments are also common, reflecting a prevalent biomedical theory that "opening" the thoracic outlet and decompressing neurovascular structures are the primary goals of intervention.

🏋️‍♂️ Rehabilitation programs are predominantly exercise-based, with stretching and strengthening being the most frequent interventions. Stretching typically targets the scalene and pectoralis muscles to increase the width of the anatomical spaces, while strengthening focuses on scapular stabilizers, such as the serratus anterior and middle-lower trapezius. Other common adjuncts include neurodynamic exercises (nerve glides), diaphragmatic breathing, postural retraining, and activity modification. Interestingly, despite the chronic nature of NTOS, only one study incorporated psychologically informed treatment, suggesting a persistent bias toward biomechanical models over holistic, biopsychosocial approaches.

🤔 The review also identified significant inconsistencies in clinical reasoning and treatment dosage. For example, there is conflicting advice regarding scapular exercises, with some authors advocating for depression and retraction and others for scapular elevation and upward rotation to avoid mechanical stress on the plexus.

In addition, the review impressively shows that the current conservative rehabilitation paradigm involves decompression and opening of the thoracic outlet through strengthening and stretching. However, it is unclear whether these interventions actually achieve this objective (e.g. a change in the position of the scapula or anatomical change in the scalenus gap).

Furthermore, while expert consensus often recommends a six-month trial of conservative care, many empirical studies utilized much shorter intervention periods, and reporting on exercise intensity and frequency remains generally poor.

💡In terms of measurement, the QuickDASH and the Cervical Brachial Symptom Questionnaire (CBSQ) are the most frequently used Patient-Reported Outcome Measures (PROMs). Prognostic data suggests that patients with less severe baseline symptoms, lower tenderness scores, and higher tolerance during provocation testing are more likely to respond successfully to rehabilitation alone. Ultimately, the authors conclude that while a vast array of techniques exists, there is a critical need for standardized, reproducible protocols co-designed by clinicians and patients to improve the evidence base for NTOS management.

12/02/2026

11/02/2026

𝗦𝗲𝗹𝗲𝗰𝘁𝗶𝘃𝗲 𝗺𝘂𝘀𝗰𝗹𝗲 𝘄𝗲𝗮𝗸𝗻𝗲𝘀𝘀 𝗶𝗻 𝗔𝗰𝗵𝗶𝗹𝗹𝗲𝘀 𝘁𝗲𝗻𝗱𝗶𝗻𝗼𝗽𝗮𝘁𝗵𝘆: 𝗶𝘀 𝗶𝘁 𝘁𝗶𝗺𝗲 𝘁𝗼 𝗹𝗼𝗼𝗸 𝗯𝗲𝘆𝗼𝗻𝗱 𝘁𝗵𝗲 𝘀𝗼𝗹𝗲𝘂𝘀?

📘 A brand-new review article by Fernandes and colleagues (https://pubmed.ncbi.nlm.nih.gov/41664282/) revisits the neuromuscular mechanisms underlying Achilles tendinopathy and questions the traditional soleus-centric explanation of plantarflexor deficits. While earlier models attributed reduced plantarflexion capacity primarily to soleus weakness, recent neurophysiological and biomechanical evidence suggests a more selective impairment within the triceps surae.

⬇️In particular, individuals with Achilles tendinopathy consistently demonstrate reduced neural drive, lower activation, and diminished force contribution of the gastrocnemius lateralis, especially during submaximal contractions (https://pubmed.ncbi.nlm.nih.gov/36418751/, https://pubmed.ncbi.nlm.nih.gov/40349309/). In contrast, soleus motor unit behaviour and force contribution appear largely preserved and may even increase as a compensatory response.

🦶 This altered coordination has important mechanical implications (graphic). Because the Achilles tendon is composed of distinct subtendons arising from each triceps surae muscle, changes in muscle-specific force sharing can modify how strain is distributed within the tendon. A reduced contribution from the gastrocnemius lateralis is therefore likely to create non-uniform strain patterns and elevated interfascicular shear stress, conditions associated with localised overload, microdamage, and maladaptive tendon remodelling. Structural findings such as selective gastrocnemius lateralis atrophy, altered muscle architecture, and reduced subtendon stiffness further support this mechanistic link. Nevertheless, whether these neuromuscular alterations precede tendon pathology or develop as protective adaptations to pain remains unresolved.

💡From a practical perspective, the review calls for a reassessment of current clinical practice. Rehabilitation approaches that focus predominantly on soleus strengthening—such as seated calf raises—may fail to address relevant muscle-specific deficits. Strategies that preferentially target the gastrocnemius lateralis, 𝗶𝗻𝗰𝗹𝘂𝗱𝗶𝗻𝗴 𝘀𝘁𝗿𝗮𝗶𝗴𝗵𝘁-𝗸𝗻𝗲𝗲 𝗹𝗼𝗮𝗱𝗶𝗻𝗴, 𝗶𝗻𝘄𝗮𝗿𝗱 𝗳𝗼𝗼𝘁 𝗽𝗼𝘀𝗶𝘁𝗶𝗼𝗻𝗶𝗻𝗴 𝗱𝘂𝗿𝗶𝗻𝗴 𝗽𝗹𝗮𝗻𝘁𝗮𝗿𝗳𝗹𝗲𝘅𝗶𝗼𝗻 (https://pubmed.ncbi.nlm.nih.gov/39985716/, https://pubmed.ncbi.nlm.nih.gov/32735428/), or biofeedback-guided activation training, may help restore more balanced force sharing within the triceps surae. However, these interventions remain hypothesis-driven, and their effectiveness for improving symptoms and function has yet to be established.

07/02/2026

Just published in “Clinical Journal of Pain” 🔥

𝗣𝗮𝘁𝗵𝗼𝗽𝗵𝘆𝘀𝗶𝗼𝗹𝗼𝗴𝘆 𝗼𝗳 𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗣𝗮𝗶𝗻

📘 Lyndon (2026, https://pubmed.ncbi.nlm.nih.gov/41614224/)

🤕 Chronic pain, defined as pain persisting beyond normal tissue healing, affects around 20% of the population and represents a major global health burden. Unlike acute pain, it no longer serves a protective function but reflects a maladaptive transformation of nociceptive processing shaped by biological, psychological, and social factors

1️⃣ Pathophysiologically, the chronification cascade emerges through interacting stages (s. illustration). It often begins with 𝗽𝗲𝗿𝗶𝗽𝗵𝗲𝗿𝗮𝗹 𝘀𝗲𝗻𝘀𝗶𝘁𝗶𝘀𝗮𝘁𝗶𝗼𝗻, where inflammatory mediators and ion-channel changes lower nociceptor thresholds, amplifying incoming nociceptive signals.

2️⃣ Sustained input then drives 𝗰𝗲𝗻𝘁𝗿𝗮𝗹 𝘀𝗲𝗻𝘀𝗶𝘁𝗶𝘀𝗮𝘁𝗶𝗼𝗻, characterised by spinal and supraspinal hyperexcitability, glial activation, reduced inhibitory control, and synaptic potentiation (“wind-up”). These processes allow pain to persist even in the absence of ongoing tissue injury.

3️⃣ With time, chronic pain induces 𝗺𝗮𝗹𝗮𝗱𝗮𝗽𝘁𝗶𝘃𝗲 𝗻𝗲𝘂𝗿𝗼𝗽𝗹𝗮𝘀𝘁𝗶𝗰 𝗰𝗵𝗮𝗻𝗴𝗲𝘀 in the CNS, altering the structure and function of nociceptive processing. Neuroimaging studies show cortical reorganisation, altered network connectivity, and impaired descending pain modulation, linking nociceptive processing with emotional and cognitive circuits.

⚖️Immune mechanisms play a central role. Neuro-immune crosstalk, driven by cytokines, glial activation, and peripheral immune-cell recruitment, sustains inflammation and neuronal hypersensitivity. Emerging work also implicates the gut microbiome, where dysbiosis may influence pain via immune and metabolic signalling.

🧠 Chronic pain is further shaped by psychosocial context. Stress, mood disorders, trauma exposure, and social adversity modulate neuroendocrine and neurotransmitter systems, altering pain perception and vulnerability. Genetic polymorphisms and epigenetic modifications add another layer, embedding environmental influences into long-term changes in gene expression.

💡Overall, the review frames chronic pain as a systems-level disorder arising from the dynamic interplay of sensitisation, neuroplasticity, immune dysregulation, and lived experience. This integrative perspective helps explain why persistent pain often outlasts its original injury and varies so profoundly between individuals.

03/02/2026

🎙️ FREE Webinar LAST CALL!

Discover what actually makes pain education effective, the challenges we face, and why getting it right matters more than ever.

📅 4 February 2026
⏰ 09:00 London | 19:30 Adelaide
🎟️ Free – https://shorturl.at/qVnlH

Whether you caught the first webinar or you're just joining us, this one's packed with insights that could shift how you approach pain education in practice.

Can't make it live? Register anyway and we'll send you the recording.

See you there! 👋