Centre de formation et physiothérapie de Lutry

04/06/2026

𝗖𝗮𝘂𝗱𝗮 𝗘𝗾𝘂𝗶𝗻𝗮 𝗦𝘆𝗻𝗱𝗿𝗼𝗺𝗲: 𝗔 2025 𝗡𝗮𝗿𝗿𝗮𝘁𝗶𝘃𝗲 𝗥𝗲𝘃𝗶𝗲𝘄

📘 In a brand-new narrative review, Conte and colleagues aim to summarise current knowledge of CES in order to help healthcare providers understand, recognise, investigate and manage CES appropriately given their local setting in the context of updated national UK guidelines (https://pubmed.ncbi.nlm.nih.gov/42053010/).

▶️ Back pain accounts for 4% of GP consultations (https://pubmed.ncbi.nlm.nih.gov/32554673/) and 2% of emergency department presentations (https://pubmed.ncbi.nlm.nih.gov/36815064/). While serious pathology underlies only 1% of cases (https://www.ncbi.nlm.nih.gov/books/NBK538173/), physiotherapists are key gatekeepers. The most critical differential is cauda equina syndrome (CES), a surgical emergency caused by acute compression of the lumbosacral nerve roots (https://www.ncbi.nlm.nih.gov/books/NBK537200/). This review updates the 2023 BJHM publication (https://pubmed.ncbi.nlm.nih.gov/38186331/) and incorporates the 2025 UK GIRFT national pathway (https://girft-interactivepathways.org.uk/cauda-equina-1/spinal-suspected-cauda-equina-syndrome-2a/) and BASS guidelines (https://spinesurgeons.ac.uk/News/7773476).

✅ Epidemiology and Aetiology
CES has a crude annual incidence of 2.7 per 100,000 in the UK (https://pubmed.ncbi.nlm.nih.gov/36315989/), with a median onset age of 58 years and a slight female predominance (https://pubmed.ncbi.nlm.nih.gov/37470755/). Prevalence rises to 18.9% in patients presenting with signs and symptoms consistent with CES (https://pubmed.ncbi.nlm.nih.gov/32059184/). Disc herniation at L4/L5 or L5/S1 is the leading cause (45% of cases), occurring in 3% of all disc herniations (https://pubmed.ncbi.nlm.nih.gov/19445754/). Pre-existing lumbar stenosis confers additional risk (https://pubmed.ncbi.nlm.nih.gov/32522648/).

✅ Pathophysiology
The cauda equina occupies 44% of the dural sac (https://pubmed.ncbi.nlm.nih.gov/29341941/). Compression reduces available space, compromising microvascular supply and leading to intraneural ischaemia, oedema, demyelination, and Wallerian degeneration (https://pubmed.ncbi.nlm.nih.gov/15131438/). Nerve regeneration following injury is limited (https://pubmed.ncbi.nlm.nih.gov/17224816/), making early recognition and decompression critical.

✅Red Flag Symptoms
Per 2025 GIRFT guidance, CES should be suspected in patients with new onset (

03/06/2026

𝐂𝐞𝐫𝐯𝐢𝐜𝐨𝐠𝐞𝐧𝐢𝐜 𝐇𝐞𝐚𝐝𝐚𝐜𝐡𝐞: 𝐓𝐡𝐞 𝐌𝐢𝐠𝐫𝐚𝐢𝐧𝐞 𝐓𝐡𝐚𝐭 𝐒𝐭𝐚𝐫𝐭𝐬 𝐢𝐧 𝐭𝐡𝐞 𝐍𝐞𝐜𝐤

​Headaches are one of the most common complaints in clinical practice, frequently labeled as Migraines or Tension-Type Headaches. However, when patients do not respond to neurological medications or stress management, the true source of the pain is often cervical: Cervicogenic Headache (CGH).

​Recent literature emphasizes that the upper cervical spine is a major, yet frequently overlooked, pain generator for unilateral headaches, largely due to the complex neuroanatomy connecting the neck and the head.

​👉 What Is a Cervicogenic Headache?
​CGH is a secondary headache disorder originating from dysfunction in the cervical spine or its surrounding soft tissues, typically involving the C1-C3 spinal segments.
​Because the nerves supplying the upper neck share a pathway with the nerves supplying the face and head, dysfunction in the neck translates into head pain.

​👉 Pathophysiology
​The mechanism relies on a critical anatomical junction: the trigeminocervical nucleus (TCN) in the upper spinal cord.
​Afferent nerve fibers from the upper three cervical nerve roots (C1, C2, C3) and the trigeminal nerve (cranial nerve V) converge here. When joints, ligaments, or muscles in the upper cervical spine are inflamed or restricted, the brain misinterprets these pain signals as originating from the forehead, eyes, or temples (the trigeminal nerve distribution).

​👉 Typical Pain Distribution
​Patients typically present with:
​• Unilateral pain that starts in the suboccipital region (base of the skull)
• Pain radiating forward to the temporal, frontal, or orbital (around the eye) regions
• A dull, non-throbbing ache that can occasionally become sharp
• Pain that is mechanically provoked by awkward neck postures or sustained reading/screen time

​👉 Key Clinical Signs
​Several clinical findings can suggest CGH over a migraine:

​✔️ Positive Cervical Flexion-Rotation Test (CFRT): A significant restriction (loss of 10 degrees or more) in upper cervical rotation when the neck is fully flexed
✔️ Pain reproduced by deep palpation of the upper cervical facet joints (C2-C3) or the greater occipital nerve
✔️ Restricted active cervical range of motion
✔️ Ipsilateral shoulder or arm pain (occasionally accompanying the headache)

​👉 Why It Is Frequently Misdiagnosed
​Because the primary symptom is head pain, it frequently mimics:

​• Migraine without aura (especially since CGH can sometimes cause nausea)
• Tension-type headaches
• Occipital neuralgia

​👉 Evidence-Based Treatment Approaches
​Treating the head won't fix a neck problem.

📌 ​Conservative management
​• Sustained Natural Apophyseal Glides (SNAGs) focusing on C1-C2 rotation
• Deep neck flexor (craniocervical flexion) strengthening to restore postural control
• Manual therapy targeting upper cervical joint mobilization
• Postural re-education to reduce forward head posture
📌 ​Interventional options
​• Diagnostic and therapeutic nerve blocks (e.g., greater occipital nerve block)
• Radiofrequency ablation of the C2-C3 facet joint nerves in severe, refractory cases

​📌 Clinical Takeaway
​If a patient complains of a one-sided headache that worsens with desk work or driving, always clear the upper cervical spine. A simple Cervical Flexion-Rotation Test can instantly differentiate a true migraine from a neck issue, guiding the patient to the right treatment rather than lifelong medication.

​✅ References
• Journal of Oral & Facial Pain and Headache, 2025 - Integration of nociceptive activity from orofacial, cranial and cervical regions in the trigeminocervical nucleus
• Validation and Test–Retest Reliability of the Cervicogenic Headache Severity Questionnaire (CeH-SeQ), 2026 - EPJ Web of Conferences

30/05/2026

Just published 🔥

𝗖𝗿𝗼𝘀𝘀-𝗲𝗱𝘂𝗰𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝘂𝗻𝗶𝗹𝗮𝘁𝗲𝗿𝗮𝗹 𝗿𝗲𝘀𝗶𝘀𝘁𝗮𝗻𝗰𝗲 𝘁𝗿𝗮𝗶𝗻𝗶𝗻𝗴 𝗮𝘀 𝗮 𝘀𝘁𝗿𝗮𝘁𝗲𝗴𝘆 𝘁𝗼 𝗺𝗶𝘁𝗶𝗴𝗮𝘁𝗲 𝗶𝗺𝗺𝗼𝗯𝗶𝗹𝗶𝘀𝗮𝘁𝗶𝗼𝗻-𝗶𝗻𝗱𝘂𝗰𝗲𝗱 𝗻𝗲𝘂𝗿𝗼𝗺𝘂𝘀𝗰𝘂𝗹𝗮𝗿 𝗱𝗲𝗰𝗹𝗶𝗻𝗲: 𝗔 𝘀𝘆𝘀𝘁𝗲𝗺𝗮𝘁𝗶𝗰 𝗿𝗲𝘃𝗶𝗲𝘄 𝗮𝗻𝗱 𝗺𝗲𝘁𝗮-𝗮𝗻𝗮𝗹𝘆𝘀𝗶𝘀

▶️ Immobilisation has been used in the treatment of upper and lower extremity injuries since ancient times in order to reduce pain, allow tissue healing, and prevent further damage (). However, modern forms of immobilisation such as casting, bracing, or surgical fixation substantially reduce mechanical loading and therefore induce rapid declines in muscle strength and muscle mass (https://pubmed.ncbi.nlm.nih.gov/19727027/, https://pubmed.ncbi.nlm.nih.gov/38895777/).

⬇️ These neuromuscular losses occur particularly quickly during the first days of immobilisation before beginning to plateau after approximately two weeks (https://pubmed.ncbi.nlm.nih.gov/36883219/). Daily strength losses of approximately 2.0% in the knee extensors and 1.2% in the elbow flexors have been reported (https://pubmed.ncbi.nlm.nih.gov/30900205/).

💡 Importantly, these early declines in strength are thought to be driven predominantly by neural mechanisms — including reductions in neural drive, motor unit excitability, and firing frequency — rather than by muscle atrophy itself (https://pubmed.ncbi.nlm.nih.gov/41106072/, https://pubmed.ncbi.nlm.nih.gov/33981206/, https://pubmed.ncbi.nlm.nih.gov/36088611/).

⬆️ Since persistent strength deficits and asymmetries are associated with an increased risk of reinjury and delayed return to sport or work (https://pubmed.ncbi.nlm.nih.gov/36965459/, https://pubmed.ncbi.nlm.nih.gov/35141554/), cross-education of the contralateral non-immobilised limb has emerged as a promising strategy to attenuate neuromuscular decline during periods of immobilisation itself.

📘 Carroll et al. (https://pubmed.ncbi.nlm.nih.gov/17043329/) showed that these contralateral strength gains reach approximately 52% of those observed in the trained limb, highlighting the importance of maximising trained limb strength to optimise the cross-education effect in the untrained contralateral limb.

💪 Effective cross-education interventions require near-maximal training intensities to maximise strength gains in the untrained limb (https://pubmed.ncbi.nlm.nih.gov/28936703/, https://pubmed.ncbi.nlm.nih.gov/37156010/, https://pubmed.ncbi.nlm.nih.gov/33984253/).

🧠 The magnitude of strength transfer is greatest when training emphasises eccentric muscle actions, which induce greater reductions in intracortical inhibition and greater increases in corticospinal excitability compared to other contraction types (https://pubmed.ncbi.nlm.nih.gov/26037804/, https://pubmed.ncbi.nlm.nih.gov/34488881/).

📘 In a brand-new study, Rodríguez-Coloma and colleagues (https://pubmed.ncbi.nlm.nih.gov/42141765/) quantified the effects of cross-education on muscle strength and size during unilateral limb immobilisation in healthy individuals. Subgroup a**lyses examined the moderating influence of training modality (i.e., eccentric, concentric, isometric, or combined), immobilisation model (i.e., proximal vs distal limb musculature), and muscle group specificity for preserving neuromuscular function.

👫 The review included eight experimental studies with a total of 189 healthy participants. In all studies, one upper limb was immobilised for 3 to 4 weeks while the opposite limb performed resistance training.

𝗠𝗮𝗶𝗻 𝗙𝗶𝗻𝗱𝗶𝗻𝗴𝘀

📊 Cross- education attenuated strength loss compared with immobilisation alone (g = 0.53, p < 0.001), with effect magnitude moderated by immobilisation location and training modality.

💪Proximal immobilisation (i.e. shoulder joint) yielded greater attenuation (overall: g = 0.62; eccentric: g = 0.82; concentric- eccentric: g = 0.68) than distal immobilisation (i.e. wrist joint, overall: g = 0.42; eccentric: g = 0.34; isometric: 43 g = 0.63).

📊 Regarding muscle size, cross education produced a small preservation effect in the immobilised limb (g = 0.19, p = 0.01). This effect was only evident in proximal immobilisation (g = 0.40) compared to distal (g = 0.06). Quantitatively, proximal effects were about 1.5 times greater than distal effects for strength, but markedly greater—about 6.7 times—for muscle size.

🧠 Possible neuroanatomical Explanation: Proximal muscles receive enhanced descending drive from the reticulospinal tract (mediating diffuse bilateral adaptations), whereas distal fine motor movements of the hand/forearm rely heavily on the corticospinal tract. This localized control restricts the cross-activation effect, rendering cross-education far less effective at protecting distal wrist musculature from structural atrophy.

📊 Strong positive associations were observed between adaptations in the trained and immobilised limbs for strength (r = 0.79) and muscle size (r = 0.81). These findings indicate that cross-education attenuates losses in muscle strength and size during immobilisation. However, these results should be interpreted with caution due to the varying risk of bias among the included studies.

💡 Several distinct neurophysiological and morphological mechanisms might explain theses results:

👉 Strength Sparing is Primarily Neural: Early strength losses during disuse are predominantly driven by neural decrements, such as reduced neural drive and altered motor unit firing rates, rather than immediate muscle atrophy. Cross-education acts as a direct countermeasure by maintaining cortical excitability and neural drive to the immobilised limb.

👉 Size Sparing is Limited by Lack of Load: Muscle hypertrophy and mass preservation are fundamentally dependent on direct external mechanical loading. Because the immobilised limb experiences no actual load, the cross-education effect on muscle size is predictably small.

👉 Potential Protein Synthesis Modulation: The small amount of muscle size preservation that does occur might be driven by sustained neural activation, which may weakly modulate local signaling pathways to abated decreases in muscle protein synthesis, effectively slowing down tissue atrophy.

𝗪𝗵𝗮𝘁 𝗮𝗿𝗲 𝘁𝗵𝗲 𝗽𝗼𝘀𝘀𝗶𝗯𝗹𝗲 𝗺𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺𝘀?

The broader neural cross-transfer of strength is justified by two primary candidate cortical mechanisms:

🧠 The Cross-Activation Hypothesis (https://pubmed.ncbi.nlm.nih.gov/23908616/): Unilateral motor training produces spillover activation facilitating neural adaptations in both hemispheres, driving concurrent neural adaptations in both the trained and untrained descending pathways.

🧠 The Bilateral Access Hypothesis: The neuroplastic adaptations remain localized within the hemisphere controlling the trained limb, but the untrained hemisphere can directly "access" these motor schemes via transcallosal pathways (the corpus callosum) when trying to recruit the immobilised limb (https://pubmed.ncbi.nlm.nih.gov/23908616/).

📋 Exercise Prescription Guidelines

1️⃣ Implement cross-education immediately during the acute immobilisation phase to blunt the steep initial drops in voluntary neural drive.

2️⃣ Prioritize Eccentric Load: Incorporate high-intensity eccentric actions (e.g., eccentric preacher curls) where feasible to optimize neuroplasticity and maximize transfer magnitude.

3️⃣ Demand Near-Maximal Intensity: Exercise prescription should utilize near-maximal intensities, as cross-education effects are highly dose-dependent.

4️⃣ Target Homologous Pairs: Ensure targeting of the exact homologous contralateral muscle groups to exploit muscle-specificity advantages.

29/05/2026

Neurological disorders are now the leading cause of disability worldwide. Yet neurology has transformed over the past two decades, reshaping disease management.

Reflecting on both the growing global burden and recent scientific progress, The Lancet has just published a special issue on neurology.

From Alzheimer’s disease to multiple sclerosis, explore a collection of:
🏥 Original clinical research,
📝 Expert commentary,
👤 Inspiring profiles

Read the full issue: http://spkl.io/618776WhV

👇 Cover of The Lancet's Special issue on Neurology.

24/05/2026

Differencial diagnosis see T4 syndrome!

Hot off the Press 🔥

𝗗𝗶𝗮𝗴𝗻𝗼𝘀𝘁𝗶𝗰 𝗰𝗿𝗶𝘁𝗲𝗿𝗶𝗮 𝗳𝗼𝗿 𝗻𝗲𝘂𝗿𝗼𝗴𝗲𝗻𝗶𝗰 𝘁𝗵𝗼𝗿𝗮𝗰𝗶𝗰 𝗼𝘂𝘁𝗹𝗲𝘁 𝘀𝘆𝗻𝗱𝗿𝗼𝗺𝗲 (𝗻𝗧𝗢𝗦)- 𝗔𝗻 𝗘𝘅𝗽𝗲𝗿𝘁 𝗖𝗼𝗻𝘀𝗲𝗻𝘀𝘂𝘀

✅ Thoracic outlet syndrome (TOS) is a group of syndromes involving the compression of neurovascular structures that traverse the thoracic outlet (https://pubmed.ncbi.nlm.nih.gov/32491382/). This thoracic outlet comprises of the subclavian vein, subclavian artery, and brachial plexus passing through interscalene triangle, costoclavicular space, and retropectoralis minor space (https://pubmed.ncbi.nlm.nih.gov/39330749/).

✅ TOS has 3 clinical categories, venous, arterial, and neurogenic, and 5 subtypes, arterial vascular, venous vascular, true neurologic, traumatic neurovascular, and disputed (https://pubmed.ncbi.nlm.nih.gov/14649631/, https://pubmed.ncbi.nlm.nih.gov/39330749/). Neurogenic thoracic outlet syndrome (nTOS) is a subset of this group of syndromes caused by brachial plexus compression (https://pubmed.ncbi.nlm.nih.gov/32491382).

✅ Although TOS itself is a rare syndrome, with an incidence of 1-3 cases per 100,000, nTOS comprises 95%-99% of TOS cases and is recognized by the Society of Vascular Surgery as the primary form of TOS (https://pubmed.ncbi.nlm.nih.gov/35963513/, https://pubmed.ncbi.nlm.nih.gov/27565596/). nTOS is more common in athletes, musicians and other professions that require an increased involvement of the upper limb and commonly presents with intrinsic hand muscle atrophy, hand weakness, neurologic sensory deficits, and non-specific pain in the upper limb.

📘 Wagner et al. (https://pubmed.ncbi.nlm.nih.gov/42169800/) used an expert Delphi consensus to identify five clinically relevant criteria for distinguishing neurogenic thoracic outlet syndrome.A panel of 20 upper extremity experts rated the importance of 54 different clinical items in reference to distinguishing nTOS. Items were ranked on a scale from 0 (least important) to 10 (most important). The mean and standard deviation for each item’s rankings were calculated.

The Cronbach alpha (a) value was used to determine the degree of concordance among the panelists’ rankings. Analogous items with similarly high rankings were combined to help develop the final criteria.

💡 The 5 criteria deemed clinically important for nTOS were:

1️⃣ 𝗮 𝗽𝗼𝘀𝗶𝘁𝗶𝘃𝗲 𝗿𝗲𝘀𝗽𝗼𝗻𝘀𝗲 𝘁𝗼 𝗶𝗻𝗷𝗲𝗰𝘁𝗶𝗼𝗻𝘀 (𝗽𝗲𝗰𝘁𝗼𝗿𝗮𝗹𝗶𝘀 𝗺𝗶𝗻𝗼𝗿, 𝗮𝗻𝘁𝗲𝗿𝗶𝗼𝗿 𝘀𝗰𝗮𝗹𝗲𝗻𝗲, 𝗺𝗶𝗱𝗱𝗹𝗲 𝘀𝗰𝗮𝗹𝗲𝗻𝗲)

Symptom relief after local anesthetic injection into the pectoralis minor, anterior scalene, or middle scalene supports nTOS.

The value of this criterion is not just “pain relief” (≥ 50% of pain or paresthesia relief as a positive result) but the localization of symptom-generating compression to either the scalene region or the pectoralis-minor/retropectoralis space.

2️⃣ 𝘂𝗽𝗽𝗲𝗿 𝗼𝗿 𝗹𝗼𝘄𝗲𝗿 𝘁𝗿𝘂𝗻𝗸 𝗿𝗮𝗱𝗶𝗮𝘁𝗶𝗻𝗴 𝘀𝘆𝗺𝗽𝘁𝗼𝗺𝘀 𝘁𝗵𝗮𝘁 𝘄𝗼𝗿𝘀𝗲𝗻 𝘄𝗶𝘁𝗵 𝘀𝘂𝗽𝗿𝗮𝗰𝗹𝗮𝘃𝗶𝗰𝘂𝗹𝗮𝗿 𝗽𝗿𝗼𝘃𝗼𝗰𝗮𝘁𝗶𝘃𝗲 𝗺𝗮𝗻𝗲𝘂𝘃𝗲𝗿𝘀

Symptoms should be reproducible in the scalene/supraclavicular region, for example by scalene pressure or Tinel sign over the scalenes. This criterion reflects suspected irritation of the brachial plexus in the scalene triangle. Worsening symptoms with the neck and shoulder movements and arm pain were combined and classified as upper trunk symptoms. Furthermore, paresthesias in the fourth and fifth fingers) and weakness in the hand were categorized as lower trunk symptoms.

3️⃣ 𝘂𝗽𝗽𝗲𝗿 𝗼𝗿 𝗹𝗼𝘄𝗲𝗿 𝘁𝗿𝘂𝗻𝗸 𝘀𝘆𝗺𝗽𝘁𝗼𝗺𝘀 𝘁𝗵𝗮𝘁 𝘄𝗼𝗿𝘀𝗲𝗻 𝘄𝗶𝘁𝗵 𝗶𝗻𝗳𝗿𝗮𝗰𝗹𝗮𝘃𝗶𝗰𝘂𝗹𝗮𝗿 𝗽𝗿𝗼𝘃𝗼𝗰𝗮𝘁𝗶𝘃𝗲 𝗺𝗮𝗻𝗲𝘂𝘃𝗲𝗿𝘀

Symptoms should be reproducible medial to the coracoid or around the coracoid/pectoralis minor region, through Tinel sign or local tenderness. This points toward possible compression in the infraclavicular or retropectoralis minor space, rather than primarily between the scalenes.

4️⃣ 𝗿𝗲𝗽𝗿𝗼𝗱𝘂𝗰𝘁𝗶𝗼𝗻 𝗼𝗳 𝗽𝗮𝗶𝗻 𝘄𝗶𝘁𝗵 90° 𝗮𝗯𝗱𝘂𝗰𝘁𝗶𝗼𝗻 𝗶𝗻 𝗲𝘅𝘁𝗲𝗿𝗻𝗮𝗹 𝗿𝗼𝘁𝗮𝘁𝗶𝗼𝗻 𝗼𝗿 𝘂𝗽𝗽𝗲𝗿 𝗹𝗶𝗺𝗯 𝘁𝗲𝗻𝘀𝗶𝗼𝗻 𝘁𝗲𝘀𝘁

Symptoms reproduced with 90° abduction/external rotation and/or symptoms reproduced with the upper limb tension test suggest neural mechanosensitivity.

5️⃣ 𝗽𝗮𝗿𝘁𝗶𝗰𝗶𝗽𝗮𝘁𝗶𝗼𝗻 𝗶𝗻 𝘄𝗼𝗿𝗸/𝗲𝘅𝗲𝗿𝗰𝗶𝘀𝗲 𝗿𝗲𝗾𝘂𝗶𝗿𝗶𝗻𝗴 𝗿𝗲𝗽𝗲𝘁𝗶𝘁𝗶𝘃𝗲 𝗮𝗿𝗺 𝘀𝘁𝗿𝗲𝘀𝘀

Repetitive overhead activity, throwing, sustained protraction, or repetitive arm stress is not diagnostic on its own. It increases plausibility when the exposure matches the symptom behavior and provocation findings.

⭕ Limitations

These diagnostic criteria should be interpreted with caution. The study is based on expert consensus rather than prospective clinical validation, and there is still no universally accepted reference standard for diagnosing neurogenic thoracic outlet syndrome.

📷illustration: Overview of the structures of the thoracic outlet.

There several important features in the thoracic outlet at the base of the neck: the scalene triangle, the costoclavicular space, and the subcoracoid (pectoralis minor) space. The scalene triangle is bounded by the anterior middle scalene muscles, as well as the 1st rib. Through this space passes the brachial plexus, which is composed of five nerve roots (C5, C6, C7, C8, and T1), as well as the brachial artery. The subclavian vein passes through the costoclavicular space, anterior to the anterior scalene muscle.

📖 Wagner, E. R., Sullivan, C. M., Cuneo, K. R., Chopra, K. N., Omole, O., Gottschalk, M. B., & Bowers, R. L. (2026). Defining Diagnostic Criteria for Neurogenic Thoracic Outlet Syndrome: An Expert Consensus. Orthopaedic journal of sports medicine, 14(5), 23259671261440925. https://doi.org/10.1177/23259671261440925

20/05/2026

How do the we use effect the preferences and beliefs of people with musculoskeletal

The authors of our latest do the deep dive ➡️ https://ow.ly/PVlm50XXLXy

14/05/2026

14/05/2026

Just published 🔥

𝗧𝗵𝗲 𝗲𝗳𝗳𝗶𝗰𝗮𝗰𝘆 𝗼𝗳 𝘀𝘁𝗿𝗲𝗻𝗴𝘁𝗵 𝗲𝘅𝗲𝗿𝗰𝗶𝘀𝗲 𝗱𝗼𝘀𝗮𝗴𝗲 𝗼𝗻 𝗽𝗮𝗶𝗻 𝗮𝗻𝗱 𝗱𝗶𝘀𝗮𝗯𝗶𝗹𝗶𝘁𝘆 𝗶𝗻 𝗽𝗲𝗼𝗽𝗹𝗲 𝘄𝗶𝘁𝗵 𝗹𝗼𝘄 𝗯𝗮𝗰𝗸 𝗽𝗮𝗶𝗻: 𝗮 𝘀𝘆𝘀𝘁𝗲𝗺𝗮𝘁𝗶𝗰 𝗿𝗲𝘃𝗶𝗲𝘄 𝗼𝗳 𝗿𝗮𝗻𝗱𝗼𝗺𝗶𝘇𝗲𝗱 𝗰𝗼𝗻𝘁𝗿𝗼𝗹𝗹𝗲𝗱 𝘁𝗿𝗶𝗮𝗹𝘀

🏋️‍♂️ Although strength exercises are recommended for for back pain (LBP) (https://pmc.ncbi.nlm.nih.gov/articles/PMC8477273/, https://pubmed.ncbi.nlm.nih.gov/40624581/), more information is needed on how to prescribe them. To date, no systematic review (SR) has investigated the impact of strength exercise parameters (e.g., intensity, frequency, sets, repetitions, exercise type, and treatment duration) on outcomes for LBP.

📘 A brand-new SR of randomized controlled trials (RCTs) by de Oliveira et al. (https://link.springer.com/article/10.1007/s00586-026-09901-5) aimed to investigate the efficacy of strength exercises dosages on pain intensity and disability in people with LBP. Comparisons of interest were placebo, sham, waiting list, and no intervention to clarify exercise efficacy.

📋 Although the review question was broad, the included evidence ultimately applied only to people with chronic non-specific low back pain; no eligible trials involved acute, subacute, radicular, or specific spinal conditions. Eight randomized controlled trials were included in the qualitative synthesis, and five contributed to the meta-a**lysis.

Main clinical finding

📊 Strength exercise showed statistically significant short-term improvements in both pain and disability compared with minimal intervention. The pooled effects were:

⬇️ Pain intensity: MD −15.89 points on a 0–100 scale, 95% CI −27.66 to −4.13
⬇️ Disability: MD −9.30 points on a 0–100 scale, 95% CI −13.80 to −4.81

✅ These effects suggest a small to moderate short-term benefit, with the pain effect approaching a clinically meaningful range depending on the threshold used. However, the certainty of evidence was low to very low, so the estimates are uncertain.

𝗗𝗼𝘀𝗮𝗴𝗲-𝘀𝗽𝗲𝗰𝗶𝗳𝗶𝗰 𝗲𝗳𝗳𝗲𝗰𝘁𝘀

🏋️‍♂️ The most consistent effects were seen for high-intensity, low-frequency, lumbar extensor-focused strength training.

▶️ 𝗛𝗶𝗴𝗵 𝗶𝗻𝘁𝗲𝗻𝘀𝗶𝘁𝘆 >60% 1𝗥𝗠

High-intensity strength exercise produced statistically significant effects:
⬇️ Pain: MD −19.3, 95% CI −27.0 to −11.6
⬇️ Disability: MD −14.2, 95% CI −15.7 to −12.8

✅ This was one of the strongest signals in the review and suggests that progressive loading above 60% 1RM may be more effective than lower-intensity strengthening for chronic non-specific low back pain.

𝗟𝗼𝘄 𝘄𝗲𝗲𝗸𝗹𝘆 𝗳𝗿𝗲𝗾𝘂𝗲𝗻𝗰𝘆: 𝗼𝗻𝗰𝗲 𝗽𝗲𝗿 𝘄𝗲𝗲𝗸

Once-weekly strength training was associated with significant improvements:

⬇️ Pain: MD −19.3, 95% CI −27.0 to −11.6
⬇️ Disability: MD −11.8, 95% CI −16.2 to −7.5

✅ Training more than once per week did not show the same consistent effect. Clinically, this may indicate that higher-load lumbar strengthening does not necessarily require high weekly frequency, possibly because recovery and tolerability are important in this population.

𝗦𝗵𝗼𝗿𝘁 𝘁𝗿𝗲𝗮𝘁𝗺𝗲𝗻𝘁 𝗱𝘂𝗿𝗮𝘁𝗶𝗼𝗻: ≤3 𝗺𝗼𝗻𝘁𝗵𝘀

Shorter programs showed significant effects:

⬇️ Pain: MD −19.9, 95% CI −26.0 to −13.8
⬇️ Disability: MD −13.4, 95% CI −15.2 to −11.6

✅ Longer interventions did not show statistically significant pooled effects, but this should not be interpreted as evidence that longer treatment is ineffective. The number of trials was small, and the evidence was imprecise.

𝗟𝘂𝗺𝗯𝗮𝗿 𝗲𝘅𝘁𝗲𝗻𝘀𝗶𝗼𝗻- 𝗲𝘅𝗲𝗿𝗰𝗶𝘀𝗲𝘀

Lumbar extension exercises showed clearer benefits than general strength training:

⬇️ Pain: MD −19.6, 95% CI −25.4 to −13.7
⬇️ Disability: MD −12.5, 95% CI −14.9 to −10.1

✅ General strength training alone showed smaller and non-significant effects in the subgroup a**lyses

⬇️ Pain: MD −8.0, 95% CI −27.5 to 11.6
⬇️ Disability: MD −3.2, 95% CI −7.8 to 1.4

✅ This does not mean general strength training is ineffective, but the available evidence more strongly supports targeted lumbar extensor strengthening.

𝗟𝗼𝗻𝗴-𝘁𝗲𝗿𝗺 𝗲𝗳𝗳𝗲𝗰𝘁𝘀

Long-term effects were not statistically significant:

⬇️ Pain: MD −9.27, 95% CI −22.83 to 4.27
⬇️ Disability: MD −2.85, 95% CI −7.13 to 1.43
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✅ Therefore, the evidence mainly supports short-term improvement, while sustained effects remain unclear.

𝗣𝗿𝗮𝗰𝘁𝗶𝗰𝗮𝗹 𝗶𝗻𝘁𝗲𝗿𝗽𝗿𝗲𝘁𝗮𝘁𝗶𝗼𝗻 💡

For physiotherapists treating patients with chronic non-specific low back pain, the review supports the use of progressive strength training, especially programs that target the lumbar extensors and reach higher relative intensities when clinically tolerated. A clinically reasonable interpretation is that once-weekly, high-intensity lumbar extensor strengthening over a period of up to 12 weeks may reduce pain by roughly 19–20 points on a 0–100 scale and disability by roughly 12–14 points on a 0–100 scale. These are meaningful short-term changes, but they should be applied with clinical reasoning because the evidence certainty is low.