Proximal hamstring tendinopathy: deep buttock pain and load management Updated 2026

Clinical synthesis based on the Goom narrative pivot (JOSPT 2016), the Cook-Purdam tendon continuum model (BJSM 2009-2016), the systematic reviews of interventions (Nasser IJSPT 2021, Dizon Sports 2023), the ICON 2019 consensus (Scott BJSM 2020) and the ESWT data (Korakakis BJSM 2018).

Proximal hamstring tendinopathy (PHT, also known in the literature as proximal hamstring tendinopathy or high hamstring tendinopathy) is an enthesis disorder affecting the common insertion of the three hamstring muscles (semitendinosus, semimembranosus and long head of biceps femoris) at the ischial tuberosity.¹ The characteristic clinical picture combines deep, well-localised pain at the gluteal fold, worsened by prolonged sitting, acceleration when running, sprinting and movements combining hip flexion with knee extension (deep lunges, hill climbing).¹,²

How is this condition defined, who does it affect and what are the risk factors?

PHT is regarded as an enthesis tendinopathy or insertional tendinopathy, distinct from mid-substance tendinopathies (Achilles, mid-portion patellar). This distinction is crucial because insertions are exposed to a particular combination of tensile loads (when the hamstrings are placed under tension) and compressive loads (compression of the tendon against bone in hip flexion), which calls for specific management strategies.³

The ICON 2019 international consensus (Scott et al. 2020 BJSM) clarified the terminology: the term tendinopathy is preferred to tendinitis (which suggests an inflammation that is absent histologically) or tendinosis (which implies a histological certainty rarely available in clinical practice).⁴ PHT therefore falls within the framework of load-induced tendinopathies.

The exact prevalence of PHT in the general population is poorly documented. The most robust data come from runner cohorts: PHT is a frequent cause of persistent posterior thigh pain in long-distance runners and sprinters, yet it remains underdiagnosed compared with acute hamstring muscle injuries.¹,⁵ A surgical case series (Lempainen 2009 AJSM) already described a mixed population of athletes and sedentary people (mean age 41 years), confirming that the condition is not confined to elite athletes.⁵

The risk factors are conceptualised in two complementary categories:¹,²,⁶

• Extrinsic factors (load): a rapid increase in volume or intensity (introducing hill sessions, sprints or interval work without progression), a change of surface (moving from track to road), a change of footwear, hard surfaces for sitting (bicycle saddle, hard bench, unpadded office surfaces).
• Intrinsic factors (individual): age (reduced tendon adaptive capacity after 40-50 years), a history of hamstring muscle injury, weak gluteal strength (compensated for by the hamstrings), restricted hip mobility (posterior capsule, limited extension), excessive anterior pelvic tilt (which increases compression of the tendon against the ischium), high BMI (increased mechanical load).

What happens inside the tendon and how does PHT evolve naturally?

The modern conception of tendinopathy as a failed healing response , and not as a chronic inflammation, is one of the major paradigm shifts of the past two decades in sports medicine.⁷ The condition is described by the continuum model of Cook and Purdam (BJSM 2009), revisited in 2016, which distinguishes three stages along a dynamic continuum:³,⁷,⁸

1. Reactive tendinopathy: a short-term non-inflammatory proliferative response after an acute overload. Tendon thickening that is reversible, driven by an increase in water and proteoglycans. No major structural change to the collagen. If load is reduced, the tendon can return to normal within a few weeks.
2. Tendon in dysrepair (Tendon Dysrepair): a more substantial attempt at healing. Disorganisation of collagen fibres, neovascularisation, hyper-innervation. An intermediate stage that is potentially reversible but requires weeks to months of controlled loading.
3. Degenerative tendinopathy: an advanced stage with areas of cell death (apoptosis), major matrix disorganisation and loss of fibrillar structure. These changes are largely irreversible but the adjacent healthy tendon can compensate (the concept of the tendon as a donut) and function can be restored despite the persistence of abnormalities on imaging.⁹

For PHT specifically, the compressive component is central: the proximal hamstring tendon wraps around the upper border of the ischial tuberosity in hip flexion, which generates a compressive load added to the traction. This compression explains why sitting (direct compression) and stretching into extreme hip flexion (compression + traction) are consistently aggravating.¹⁰ This is why initial rehabilitation programmes keep the hip close to neutral, and hip flexion is only progressively reintroduced once tolerance allows.

The natural history without adequate management is typically one of fluctuating chronic pain, with quiet periods followed by flares when load increases or sitting is prolonged. Spontaneous recovery is rare, particularly at degenerative stages. The main functional consequence, beyond the sporting impact, is intolerance to sitting, which can limit desk work, driving and social life (cinema, restaurants).¹

The diagnosis of PHT is essentially clinical.¹ No single test taken in isolation has sufficient sensitivity and specificity; it is the combination of a suggestive history and concordant provocation tests that establishes diagnostic confidence. Imaging is not required first line when the picture is typical, but it becomes useful in cases of doubt, of treatment failure, or to rule out serious alternative diagnoses such as a partial or complete avulsion.¹,²

Which questions should you ask to understand the patient and their history?

The history is the most discriminating step. Five elements should be sought systematically:¹

• Precise location: the patient typically points with a single finger to the bone of the buttock (ischial tuberosity), often described as \"in the gluteal fold\" or \"just under the buttock when I sit down\". Unilateral presentation is the rule. Pain running down the posterior thigh should prompt consideration of a differential diagnosis.
• Aggravation with prolonged sitting: this is the most discriminating element. The patient reports increasing pain after 20-30 minutes in the car, at the cinema, at the desk, or on a hard seat. Many use a cushion, shift their weight or change position regularly.¹,²
• Aggravation with energy-storage activities: acceleration when running, sprinting, uphill running, deep lunges, deadlifting, changes of direction. Patients often notice that \"slow jogging\" is fine but that as soon as they try to accelerate, the pain returns.
• Insidious mode of onset: most often progressive over a few weeks, linked to a recent change in training (volume, hills, interval work, surface). Acute onset with bruising should raise the suspicion of an avulsion or a myotendinous injury.
• Behaviour over 24 hours: little pain at rest; moderate morning stiffness; warm-up pain at the start of a run that eases then returns after exercise.

Which clinical tests should be performed and which other conditions must be ruled out?

Three provocation tests are considered the most useful for reproducing the patient's familiar pain by loading the proximal tendon:¹,³

• Puranen-Orava test (active stretch): patient standing, foot on a high support (hip flexed to about 90°), knee extended, patient leans forwards. Reproduces pain at the tuberosity through active stretch.
• Bent-Knee Stretch Test (BKS): patient supine, hip and knee maximally flexed, the examiner rapidly takes the limb into maximal hip flexion + passive knee extension. Reproduces pain through maximal passive stretch.
• Modified Bent-Knee Stretch Test (MBKS): a slower, more controlled variant of the BKS, considered more sensitive and better tolerated. Reproduces pain through progressive stretch.³

Direct palpation of the ischial tuberosity often reproduces the pain, but this test lacks specificity: the area is tender in many asymptomatic people (ischiogluteal bursitis, anatomical variation). Side-to-side comparison is essential.¹,⁴

The differential diagnosis is crucial in the deep gluteal region, a complex anatomical crossroads:¹,⁵

• Acute or subacute proximal avulsion: an often identifiable traumatic mechanism (sprinting, slipping into the splits, a fall), extensive bruising of the posterior thigh, a prognostic strength deficit (> 30%), intense acute pain. If suspected, urgent MRI because a complete avulsion may benefit from early surgery.⁶
• Deep gluteal syndrome: compression of the sciatic nerve in the subgluteal space. Characteristic feature: paraesthesia or numbness along the sciatic distribution, pain worsening on sitting but with a neurological component. Neural provocation tests (SLR, slump test) are often positive.⁷
• L5-S1 lumbar radiculopathy: a lumbar history, ascending pain, neurological signs (motor deficit, hypoaesthesia, reflex asymmetry). Lumbar examination and neurodynamic tests are essential.
• Hip disorders: femoroacetabular impingement (FAI), osteoarthritis, labral tear. Pain is often inguinal or follows the \"C-sign\" pattern, with positive FADIR/FABER tests. Radiographs and MRI if needed.⁸
• Proximal gluteal tendinopathy: lateral trochanteric pain, not ischial. Different provocation tests (Trendelenburg, single-leg stance).
• Isolated ischiogluteal bursitis: rare in isolation, more often associated with the tendinopathy. Ultrasound can help.

The role of imaging is second line:¹,⁹

• MRI: the reference standard. It demonstrates tendon thickening, intratendinous oedema (T2 hyperintensity), peri-ischial bone oedema (sometimes) and partial tears. It rules out an avulsion and quantifies the chronic component. Limitation: abnormalities are present in 50% of asymptomatic people (corrected Zissen 2010 AJR), so interpretation must be made in clinical correlation.¹⁰
• Ultrasound: less sensitive than MRI for oedema but useful for visualising thickening, Doppler neovascularisation and the adjacent bursae. Operator-dependent. It allows injections to be guided.
• Radiography: of little value for the tendon but useful for ruling out a calcification, an adolescent bony avulsion or hip involvement.

Should patients be classified by their stage on the tendon continuum?

Yes: not to produce a rigid \"label\", but to tailor the load management strategy.⁷ The clinician tries to place the patient on the continuum:

• Reactive stage: young athlete, recent symptoms (< 4-6 weeks), triggered by an identifiable acute rise in load. The tendon is often swollen. Priority: temporary reduction of the aggravating load (compression and energy storage), then progressive reintroduction over a few weeks.
• Dysrepair or degenerative stage: older patient, long history (months to years), previous treatment failures. Priority: progressive heavy mechanical stimulus (HSR) to improve tendon capacity, rather than prolonged rest.

This logic explains a clinical paradox: a heavy loading programme applied too early to a reactive tendon can worsen symptoms, whereas a simple reduction in load is not enough for a degenerative tendon that needs a mechanical stimulus in order to adapt.¹,⁷

The management of PHT rests on three principles: (1) load management (temporary reduction of compressive and energy-storage loads), (2) a structured strengthening progression (isometrics, then heavy slow, then plyometric), and (3) the cautious addition of adjuncts when progress plateaus (shockwave therapy first, injections as a last resort).¹,²,³

Where do you start? What is the hierarchy of interventions?

The consensus treatment pyramid always places education and load modification in the first line:¹,⁴

• Modify the sitting position: use a \"donut\" cushion or a gel cushion, sit on the edge of the seat (transferring pressure to the thighs), avoid prolonged sitting on hard seats, take standing breaks every 30-45 minutes.
• Temporarily avoid provocative stretching: classic stretches into full hip flexion (hands-to-toes, seated straight-leg stretches) increase compression. To be avoided in the initial phase, then reintroduced cautiously from phase 3 onwards.³
• Reduce the volume of energy-storage activities: sprints, hills, climbs and deep lunges are temporarily limited. \"Slow jogging\" on flat ground can be maintained if it is well tolerated.
• Education: explain the non-inflammatory overload nature of the problem, the potentially chronic course, and the importance of adhering to the progression (typically 3-6 months).

The complete-rest approach is harmful : it weakens the tendon further and increases the risk of re-exacerbation when activity resumes. The rule is: load without aggravating, guided by 24-hour pain monitoring (the Silbernagel rule).⁵

What is the place of progressive exercise and which phases does it comprise?

Progressive exercise is the intervention best supported by the evidence, although the overall quality of the studies remains moderate (the systematic reviews of Nasser 2021 IJSPT and Dizon 2023 Sports identify a lack of high-quality RCTs but a consistency of findings favouring progressive loading for pain and function).⁶,⁷ The sequence recommended by Goom 2016 has become the de facto clinical standard:¹

A few clinical points on each phase:

• Phase 1 (isometrics): closed-chain isometrics with the hip close to neutral (basic glute bridge) allow the posterior chain to be activated without compression against the ischium. Contractions are long (30-45 sec), repeated 5 times, 2-3 times a day. The post-isometric analgesic effect observed in other tendinopathies (patellar tendon) is sometimes cited for PHT by extrapolation, without specific direct high-level evidence.⁸
• Phase 2 (HSR): Heavy Slow Resistance (3 sec eccentric + 3 sec concentric) with increasing loads (RPE 7-8/10) is now the dominant approach. The exemplary case report by Krueger 2020 (a 31-year-old powerlifter) describes a 12-week progression leading to a return to the pre-injury level and beyond.⁹ Typical exercises: Romanian deadlift, single-leg deadlift, dumbbell hip thrust, machine leg curl. Range of motion is limited initially (avoiding maximal hip flexion), then widened.
• Phase 3 (energy storage and release): only for patients who need to run or jump. Graded plyometrics: A-skips → bounding on the spot → forward bounding → jump lunges. This phase is not required for sedentary patients.
• Phase 4 (return to running): low-intensity straight-line running → increasing volume → increasing intensity → short sprints → changes of direction. Running cadence can be increased by 5-10% to reduce compressive forces on the tendon (Lenhart 2014 JOSPT).¹⁰

Shockwave, injections, adjunctive therapies: what is the real efficacy?

Adjunctive modalities never replace a well-conducted exercise programme. They may be considered when progress stalls at 8-12 weeks.¹,²

• Extracorporeal shockwave therapy (ESWT): the systematic review by Korakakis 2018 BJSM (52(6):387-407) on lower limb tendinopathies concludes that ESWT is a reasonable option for chronic tendinopathies, including PHT. The pivotal RCT by Cacchio 2011 AJSM (39(1):146-153) in 40 professional athletes with chronic PHT showed superiority of radial shockwave therapy (4 sessions, 2500 impulses) over traditional conservative treatment at 12 months (success: 85% vs 10%).¹¹,¹² Caveat : a small, single-centre study in a specific population of professional athletes.
• Ultrasound-guided corticosteroid injections: may provide short-term relief (4-6 weeks; Zissen 2010 AJR reported 50% relief lasting > 1 month). However: increased risk of tendon rupture, not recommended routinely, to be reserved for exceptional cases (rehabilitation impossible for occupational reasons or immediate competition).⁵,¹³
• Platelet-rich plasma (PRP): data specific to PHT are limited. For tendinopathies in general, recent meta-analyses do not demonstrate robust superiority over placebo in good-quality RCTs.¹⁴ Not to be recommended routinely.
• Manual therapy, dry needling, transverse frictions: may be used as adjuncts for pain modulation, but without evidence of specific efficacy for PHT. Dry needling has sometimes been used as a complement (Jayaseelan 2014 JOSPT).¹⁵
• Relative rest, ice, systemic NSAIDs: NSAIDs can be used occasionally during an acute flare, but their chronic use is harmful (inhibition of tendon healing). Complete rest is contraindicated.

Beyond the physical: how do you educate the patient and address psychological factors?

Education is a therapeutic tool in its own right, not a \"bonus\". Three key messages should be conveyed:¹,⁶

• Pain is not a precise \"tissue alarm signal\" : pain of 4/10 during exercise does not mean that things are getting worse. The rule is: acceptable pain during exercise + no worsening at 24 hours = carry on.
• Recovery takes a long time : 3-6 months on average for significant improvement; 9-12 months for chronic cases. Setting realistic expectations prevents discouragement and drop-out.
• Adherence is the number 1 predictor of success : a patient who completes 80% of their programme is twice as likely to improve their VISA-H as a patient who completes 30%.¹⁶

Psychosocial factors to screen for:

• Kinesiophobia (fear of movement): Tampa Scale of Kinesiophobia (TSK), clinical threshold > 37.
• Catastrophising : Pain Catastrophizing Scale (PCS), clinical threshold > 30.
• Limiting beliefs : \"my tendon is damaged, I will never be able to run again\". To be challenged with the evidence on tendon plasticity (Bohm 2015 Sports Med Open) and the success stories in case reports (Krueger 2020).

The long-term management of PHT does not stop when pain disappears. It aims to restore a load capacity greater than functional demands, which is the condition for preventing recurrence.¹ The exact recurrence rate is not robustly established for PHT (few long-term prospective studies), but clinical experience and analogies with other tendinopathies suggest a persistent vulnerability of the tendon, particularly to load spikes.²

How can the patient be made an active partner in recovery through self-management?

Patient empowerment rests on three pillars: (1) understanding the condition, (2) self-monitoring of the response to load, and (3) the ability to modulate their activities according to that response.¹,³

Silbernagel's 24-hour rule: the key self-monitoring tool

Initially validated on the Achilles tendon (Silbernagel 2007 AJSM), the 24-hour rule is today applied by extrapolation to most tendinopathies, including PHT:⁴

• Acceptable pain during exercise: VAS ≤ 4/10.
• Acceptable pain after exercise: no worsening the next day compared with baseline.
• Acceptable pain on palpation: return to baseline within 24 hours.

If one of these criteria is exceeded: reduce the volume or intensity of the next session by 10-20%. If all are met: consider progressing. This system turns the patient into the \"co-pilot\" of their rehabilitation.⁴

Pacing: avoiding the boom-bust cycle

Pacing is the art of dosing activity to avoid peaks followed by crashes (the boom-bust) :⁵

• Identify the \"tolerable baseline\" : the daily activity volume that generates no worsening the next day.
• Increase in 10% steps : follow the rule of a maximum 10% weekly increase in running volume.
• Schedule active recovery days: 1-2 days a week without running but with HSR exercises maintained.
• Manage occasional spikes (competition, an unplanned hike) with a planned load reduction over the following 2-3 days.

Education about the non-linear nature of recovery

The improvement trajectory is rarely linear. The patient must be prepared for occasional painful flares, which do not mean a relapse if they stay within the limits of the 24-hour rule. Picturing progress as \"two steps forward, one step back\" reduces anxiety and drop-out.¹

When and how should a safe return to sport and running be planned?

Return to sport (RTS) must never be dictated by a fixed calendar.⁶ A premature return, based solely on the disappearance of pain at rest, is the number 1 risk factor for recurrence. RTS planning relies on objective functional criteria, following the logic of the BAMIC framework (British Athletics Muscle Injury Classification) developed for muscle injuries (Macdonald 2019 BJSM) and applicable by analogy to tendinopathies.⁷

Prerequisite criteria for a partial return

• No pain on palpation of the ischial tuberosity (or pain < 2/10 side to side).
• Full tolerance of HSR exercises at a load equivalent to pre-injury or to the healthy side.
• Isometric strength symmetry in hip extension (deficit < 10%), measured with a hand-held dynamometer.
• Tolerance of plyometric exercises at a basic level (A-skips, bounding on the spot) without a delayed reaction.
• VISA-H > 80/100 or an improvement of ≥ 20 points from baseline.

Phases of reintroduction to sport

1. Straight-line running, low intensity (60-70% max HR): start at 1.5-3 km, then +10% per week according to tolerance. 3 sessions a week.
2. Moderate-intensity running (70-85% max HR): introduction of short accelerations (15-30 m).
3. Progressive sprints: short sprints (30 m), then increasing length, then increasing intensity (80% → 90% → 100%).
4. Changes of direction, agility work: the final stage, with maximal multidirectional demands.
5. Reintegration into team training : controlled portions (warm-up, technical drills) before game situations.

\"Taping the window\": maintaining HSR even after the return

Athletes returning to competition must maintain 1-2 HSR sessions a week as prevention. The tendon does not \"heal\" by becoming what it was before; it remains more vulnerable and requires continuous maintenance of its load capacity.¹,³

Clinical cases are a valuable source of learning for the clinician: they show how general principles take shape in individual trajectories, and bring to light subtleties that standardised protocols do not capture. All the cases presented here are peer-reviewed publications with a searchable PMID.

Analysis of a \"classic\" case: a long-distance runner (Campos-Villegas 2024)

The case report by Campos-Villegas et al. published in the International Journal of Sports Physical Therapy in 2024 describes the management of a 30-year-old recreational runner with deep right buttock pain that had come on insidiously after a 10 km race.¹ Symptoms were aggravated by running on sloping ground and by prolonged sitting, particularly while driving.

Diagnostic approach: palpation reproducing pain at the ischial tuberosity, positive provocation tests (Puranen-Orava, Bent-Knee Stretch), no neurological signs. Clinical diagnosis of PHT made without initial imaging.

Rehabilitation programme: a progressive loading protocol over several phases, including initial isometric exercises, then controlled eccentric and concentric strengthening, with assessment by the VISA-H score. The progression incorporated the 24-hour rule to adjust loads.¹

Results: a progressive return to running after several weeks of rehabilitation, with significant improvement in VISA-H and in functional tolerance. The case illustrates the value of an individualised progression that respects the principles of load management.¹

The diagnostic challenge: when PHT coexists with other conditions

The case report by Lewis 2020 (Journal of Chiropractic Medicine) describes a 53-year-old Tae Kwon Do athlete, who had practised for 10 years and had stopped all activity for a year because of chronic, insidious-onset pain in the left buttock, radiating to the hip and posterior thigh.² Initial pain score: 7/10. Major functional impact (brisk walking, sitting).

Diagnostic approach: radiographs of the lumbopelvic complex were negative. Clinical examination localised the pain to the left ischial tuberosity. MRI revealed bilateral trochanteric bursitis + left hamstring tendinopathy.

Management: a conservative approach combining therapeutic ultrasound over the hamstring enthesis, manual sacroiliac manipulation, and progressive rehabilitation. Complete resolution of symptoms.

Lessons: this case illustrates two crucial points:

• The combination of conditions is common in veteran athletes (female, age, repeated stress). The clinician must look beyond the symptomatic tendon alone.
• The associated sacroiliac dysfunction can increase the stresses on the ischial enthesis and must be addressed in parallel.²

Complex case studies: a powerlifter on HSR and an elite tennis player on pain monitoring

Case A: a competitive powerlifter on Heavy Slow Resistance (Krueger 2020 IJSPT)

This case report describes a 31-year-old powerlifter with chronic PHT, with pain at the ischial tuberosity and hip weakness limiting his lifts and preventing him from sitting for more than 30 minutes.³

Programme: 12 weeks of targeted Heavy Slow Resistance, with progression of the load intensity. The main exercises were lifting variations (squat, deadlift) with controlled range of motion and slow tempo.

Results:

• Marked reduction in pain from week 4 onwards.
• At 12 weeks: performance exceeding the pre-injury level (100 kg back squat, 160 kg conventional deadlift, 90 kg Romanian deadlift).
• No recurrence at 1-year follow-up.³

This case demonstrates that heavy load ≠ dangerous in tendinopathy. On the contrary, in a well-selected patient (young, motivated, strength athlete), HSR is the most effective intervention for raising tendon capacity beyond the pre-injury level.

Case B: an elite tennis player with the pain-monitoring model (Petersen 2022 JOSPT Cases)

This case report published in JOSPT Cases describes the application of the pain-monitoring model in a 24-year-old elite tennis player with right-sided PHT.⁴ The model had initially been validated on the Achilles tendon (Silbernagel 2007) but had never been the subject of a dedicated publication for PHT.

Approach: rehabilitation based mainly on progressive strengthening exercises and training load management guided by the pain-monitoring model (acceptable pain ≤ 5/10 during exercise AND no worsening the next day).

Results after 24 weeks:

• Return to unrestricted training.
• VISA-H: 76/100 (baseline not reported, but a clear improvement).
• OSTRC severity score: 0 (asymptomatic).⁴

This case validates the extrapolation of the Achilles pain-monitoring model to PHT and illustrates the importance of regular self-assessment by the elite patient.

Critical notes on clinical cases in PHT

Several limitations must be kept in mind when interpreting case reports:

• Publication bias: published cases tend to be success stories. Patients whose rehabilitation fails are under-represented.
• Limited generalisability: a protocol that succeeded in a 31-year-old powerlifter (Krueger 2020) does not apply as it stands to a 55-year-old female runner with hypermobility.
• No control group: it is impossible to attribute the improvement formally to any particular intervention.
• Heterogeneity of outcomes: some report VISA-H, others VAS, others sport-specific performance. The Nasser 2021 IJSPT meta-analysis highlights this lack of standardisation which complicates synthesis.⁵

Integrating evidence into daily practice is the main challenge for the modern physiotherapist. Beyond technical knowledge, excellence rests on the capacity for clinical reasoning, on interprofessional collaboration and on objective measurement of outcomes.

When and to which other professionals should you refer?

The direct-access physiotherapist plays a key triage role. Vigilance for red flags is the most critical safety skill:¹

• To the emergency department, or urgently to the GP: acute trauma with a mechanism of slipping into the splits, extensive bruising of the posterior thigh, major motor deficit → suspicion of acute proximal avulsion. MRI within ≤ 7 days and an orthopaedic surgical opinion. A complete avulsion in an active person may benefit from early surgical repair (Lempainen 2009).²
• To the orthopaedic surgeon / sports physician: failure of well-conducted conservative treatment over 6-12 months; suspicion of an unoperated partial avulsion documented on MRI; refractory disabling pain in a person wishing to return to competition.
• To the rheumatologist / physician in internal medicine: an atypical picture (bilateral pain of simultaneous onset, systemic signs, inflammatory context) → rule out a spondyloarthropathy or an axial-peripheral enthesopathy.
• To the neurologist: associated neurological signs (L5/S1 sensory deficit, motor deficit, saddle anaesthesia) → rule out a compressive radiculopathy or cauda equina syndrome.
• To the psychologist / pain specialist: predominant psychosocial factors (catastrophising, kinesiophobia, anxiety, depression). A biopsychosocial approach combining CBT and exercise is superior to either approach alone for chronic musculoskeletal pain.³,⁴
• To the podiatrist / biomechanist: a runner with objectively measurable biomechanical faults (excessive overpronation, marked overstriding). Running analysis and possible orthotic adjustment can reduce the stresses on the enthesis.

How do you measure outcomes and overcome barriers to implementation?

Recommended objective measures

Progress assessment must be standardised, multidimensional and reproducible:⁵

• VISA-H (Victorian Institute of Sport Assessment: Hamstring): a questionnaire validated in 2014 by Cacchio (BJSM), 8 items, score 0-100 (100 = asymptomatic). Sensitive to change. Available in French (Causeret 2019).⁵
• Sit-to-pain duration : the maximum tolerable sitting time without pain > 2/10. A simple measure, representative of functional impact.
• Isometric hip extension strength test : hand-held dynamometer, supine with the hip flexed to 30° / 60° / 90°. Allows side-to-side symmetry to be tracked.
• VAS / NPRS : pain on palpation, the patient's typical running pain, post-exercise pain.
• OSTRC severity score (Oslo Sports Trauma Research Center): for athletes, assesses the impact on sports participation.

Understanding the GRADE pyramid of evidence

The GRADE system (Grading of Recommendations, Assessment, Development and Evaluation) is the international reference scale for appraising the quality of evidence. It distinguishes four levels of certainty:⁶

Barriers to implementation, and levers

The common barriers to evidence-based practice in physiotherapy have been documented:

• Lack of time for collecting PROMs → build it into the welcome time or before the session with a paper form or a dedicated app.
• Difficulty interpreting studies → take part in journal clubs, follow critical summaries (Physio Network, La Clinique Du Coureur, Bjsmclub).
• Weak organisational support → promote outcome measurement to patients and payers as a quality indicator.
• Resistance to changing practice → mentoring by experienced clinicians and specialised continuing education are powerful levers.

Shared decision-making: bringing in the patient's values

Evidence-based practice is not the mechanical application of recipes. It brings together three equal components : (1) the best available evidence, (2) the physiotherapist's clinical expertise, and (3) the patient's values and preferences. A powerlifter patient will prefer heavy HSR; an older sedentary patient will prefer a gentler programme. The clinician adapts without betraying the spirit of the approach.

CTA section: take the next step