Clinical synthesis based on the McDevitt 2022 international Delphi, the BMC 2023 scoping review, the Clin Orthop 2025 prospective data and the Cook & Purdam, Hegedus and Coombes meta-analyses.

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

Long head of biceps tendinopathy, abbreviated LHB or LHBT in the English-language literature, corresponds to an essentially degenerative disorder of the tendon in its intra-articular and bicipital portion, with disorganisation of the collagen fibres, increased ground substance and neovascularisation. Histopathology shows little or no acute inflammation, which justifies abandoning the historical term “tendinitis”.¹ ²

The condition is rarely isolated. A scoping review published in 2023 in BMC Musculoskeletal Disorders concludes that the great majority of long head of biceps disorders coexist with rotator cuff pathology, and surgical series report comorbidity in up to 93% of cases.² ³ Primary tendinopathy (direct mechanical impingement in the bicipital groove) is classically distinguished from secondary tendinopathy, which is far more frequent and stems from instability or lesions of adjacent structures.

A prospective study published in Clinical Orthopaedics and Related Research in 2025 (n = 500 symptomatic adult shoulders, mean age 55 years, 49% men) quantified the effect of age for the first time: the prevalence of long head of biceps abnormalities on MRI rises by about 4% per year of age and remains strongly linked to concomitant cuff tendinopathy.⁴ This finding refocuses the clinical reading: LHB tendinopathy is above all a marker of global degeneration of the subacromial complex. 🧓

The risk factors can be classified into two categories:

• Extrinsic : repetitive overhead sports (throwing, swimming, tennis, volleyball, weightlifting), sudden increase in training load, subacromial impingement, anterior glenohumeral instability and repetitive overhead manual work.⁵ ⁶
• Intrinsic : zone of relative hypovascularity in the intra-articular portion (critical zone of Refior & Sowa, described in 1995), morphology of the bicipital groove (shallow, medial spur overhang), subscapularis weakness, scapular dyskinesis, ageing and hormonal status (post-menopause).⁵ ⁷ ⁸

What happens in the body and how does long head of biceps tendinopathy evolve?

The pathophysiology follows the continuum model proposed by Cook & Purdam in 2009 in the British Journal of Sports Medicine, a model that still structures the clinical reading of tendinopathies at all sites today.⁹ Three stages:

1. Reactive tendinopathy : a non-inflammatory proliferative response to acute overload. The tendon thickens transiently to reduce stress. This stage is reversible if load is managed.⁹ 📈
2. Remodelled tendon (dysrepair) : a disorganised healing attempt, with increased proteoglycans, fibre separation, neovascularisation and increased innervation contributing to chronicity.²
3. Degenerative tendinopathy : irreversible structural changes, cell apoptosis, marked collagen disorganisation. Increased risk of partial or complete rupture.⁹ ¹⁰ 📉

The untreated natural course tends towards chronicity in a substantial fraction of cases, with worsening of associated cuff lesions, tendon weakening and risk of spontaneous rupture (classic manifestation: “Popeye sign”). Conversely, when a complete rupture occurs on an advanced tendinopathy, the functional consequences are often modest (loss of 8-20% of strength in supination and elbow flexion depending on the series) because the short head and the supinator partially compensate.¹¹

How do you assess and diagnose long head of biceps tendinopathy with certainty?

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The diagnosis of LHB tendinopathy is above all a diagnosis of correlation : anterior shoulder pain is non-specific and the reliability of clinical tests taken in isolation is limited.¹ ² The best strategy combines careful history-taking, a battery of at least two to three tests that provoke pain in the bicipital groove, differential diagnosis manoeuvres and, if necessary, targeted imaging.

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

The history should explore several areas 🤔:

• Location : anterior pre-deltoid pain, classically in the bicipital groove, sometimes radiating towards the biceps brachii.³
• Mechanism : gradual onset (overuse, overhead sport) vs acute onset (effort in supination against resistance, trauma).
• Joint noises : clicks (popping) or snapping during glenohumeral rotations → suspect tendon instability, pulley lesion or subscapularis rupture.⁴
• Aggravating factors : overhead movements, carrying loads, supination against resistance, sleeping on the affected side.
• History : glenohumeral dislocations, trauma, previous injections, chronic overhead sports, manual occupation.
• Yellow flags : kinesiophobia, low self-efficacy, negative expectations. Chester 2018 (BJSM, n = 1030) showed that these psychological variables are stronger predictors of physiotherapy outcome than the structural clinical examination.⁵

Which clinical tests should you perform and which other conditions need to be ruled out?

The reference meta-analysis by Hegedus (BJSM 2012, updated 2017) concluded that no single test has sufficient diagnostic value to confirm or exclude LHB involvement.¹ ² The reasonable strategy is to combine several tests and palpation. A recent diagnostic study in a surgical population (Erickson 2019) confirmed that in a cluster, the Upper Cut + palpation give the best characteristics (sensitivity 88% in parallel, specificity 93% in series).⁶ ⁷

Differential diagnosis: a non-negotiable step 🎯

The high prevalence of concomitant pathologies requires a structured approach:

• Subscapularis rupture : the tendon forms the roof of the biceps pulley; its rupture is the major mechanical cause of LHB instability. The Belly-press and the Lift-off should be performed systematically.⁸
• SLAP lesion (biceps anchor): the Biceps Load II (Kim 2001, n = 127) remains the best-performing single test (sens 89.7%, spec 96.9%).⁹ These original values have not been replicated: in a study with strict methodological controls, the positive likelihood ratio of the Biceps Load II falls to 1.7.
• Subacromial impingement : Neer and Hawkins-Kennedy can provoke pain referred to the groove without primary LHB involvement.
• Suprascapular nerve entrapment at the spinoglenoid notch: posterolateral pain, possibly anterior, weakness of external rotation, infraspinatus atrophy. To be considered if conservative treatment unexpectedly fails.¹⁰
• C5-C6 radiculopathy : cervicobrachial pain, motor or sensory deficit, positive Spurling.

Imaging

• Dynamic ultrasound : first-line examination. Assesses thickening, tenosynovitis and subluxation on rotation. Operator-dependent.¹¹ ¹² For partial rupture, its sensitivity ranges from 0.27 to 0.71 (four studies), although the authors consider ultrasound reliable to confirm as well as to exclude all LHB disorders.¹⁷
• MRI : highly specific for complete LHB rupture (93 to 99%), with more variable sensitivity (56 to 90%); for tendinosis and partial rupture, sensitivity 68% and specificity 76% (negative likelihood ratio 0.44): a normal MRI does not rule out the disorder.¹⁶ It remains useful for neighbouring structures: the cuff, whose tears it detects as well as ultrasound does (MR arthrography doing better),¹³ the labrum and the bone.
• MR arthrography : useful when a SLAP lesion or a refractory pulley is suspected.

Should patients with long head of biceps tendinopathy be classified?

Yes: classification improves interprofessional communication, guides treatment and refines prognosis. A scoping review published in 2025 (PMID 40606699) catalogued all the existing systems (Walch, Habermeyer, Lafosse, Boileau, Itoi, Bennett) and proposed a new 4-stage arthroscopic classification (A: normal, B: erythema, C: fraying, D: labral involvement).¹⁴

For physiotherapy clinical practice, the functional classification by anatomical zone is the most operational:

1. Zone A: extra-articular (bicipital groove) : tendinopathy, tenosynovitis. Good response to conservative treatment (exercise, MT, education).
2. Zone B: junction / pulley : lesion of the reflection pulley (Habermeyer / Bennett), often associated with partial rupture of the subscapularis and supraspinatus. Cause of instability (subluxation, dislocation). Treatment often surgical.¹⁵
3. Zone C: intra-articular : SLAP lesion, involvement of the biceps anchor. Strategy depends on age, activity and severity.

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

Conservative treatment is the undisputed first line. The McDevitt international Delphi (Int J Sports Phys Ther 2022, 29 experts) established a consensus on 61 recommended interventions for LHB tendinopathy, organised around four pillars: education, therapeutic exercise, adjunct manual therapy and load management.¹ The consensus recommends maintaining the conservative approach for at least 12 weeks before any surgical escalation (tenotomy or tenodesis).¹ ²

What is the place of exercise, and is there a superior approach?

Exercise is the central pillar and the most consensual intervention (McDevitt 2022 strong recommendation). No modality has demonstrated absolute superiority, but effective programmes share:

• Progressive loading : isometric (analgesia, Rio 2015) → heavy slow isotonic strengthening (HSR, Kongsgaard / Beyer) → ballistic / plyometric for overhead athletes.³ ⁴ ⁵
• Rotator cuff strengthening : essential because humeral centring determines the mechanical load on the LHB.⁶
• Scapular control : lower trapezius, serratus anterior; scapular dyskinesis is a major contributing factor in painful shoulders.⁶ ⁷
• Pain tolerance : a practice benchmark, pain ≤ 4/10 during exercise, stable or decreasing within 24 h, in order to progress the load; Smith 2017 does not validate this threshold, it shows a small short-term benefit of exercises that allow pain (moderate certainty).⁸

Manual therapies, technologies: how effective are they really?

• Corticosteroid injections : the landmark meta-analysis by Coombes (Lancet 2010, 41 RCTs) remains the reference: short-term benefit (4-8 weeks), but results equivalent to or even worse than placebo in the medium and long term, and a cumulative risk of tendon weakening. To be reserved for very painful cases as a complement to an exercise programme, ideally ultrasound-guided.⁹
• Extracorporeal shockwave therapy (ESWT) : the Brindisino meta-analysis (Physiotherapy Research International 2024, 21 RCTs) finds shockwave therapy better than a sham on pain and function in the calcific cuff at 24 weeks, and less good than ultrasound-guided needling, with very low certainty. Data on isolated LHB tendinopathy are lacking; extrapolation, when cuff comorbidity is established, remains a hypothesis.¹⁰
• Manual therapy : glenohumeral, scapulothoracic and thoracic mobilisations, soft-tissue release of the subscapularis. Modest but consistent benefit in addition to exercise (never replaces exercise).¹¹
• Physical modalities (TENS, laser, ultrasound): low to very low level evidence, of symptomatic interest only.

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

Education is a treatment in its own right, not a supplement. Three priority areas:

1. Explaining the condition : tendinopathy is a problem of load capacity, not a “tear” or “irreversible damage”. This reframing reduces kinesiophobia.¹² ¹³
2. Active load management : pacing, planning, alternating phases of stress and recovery. Tools: activity diary, smartphone app.
3. Adherence to the exercise programme : the patient must understand that it is the main intervention and that the benefits are progressive (4 to 12 weeks before the peak effect).

Chester 2018 (BJSM, n = 1030) showed that psychological factors (self-efficacy, recovery expectations, severity of rest pain) are more strongly associated with the outcome than structural clinical signs.¹³ Taking account of kinesiophobia (TSK-11), catastrophising (PCS) and depression (PHQ-9) must be part of the initial assessment.

Why are more than 90% of LHB tendinopathies associated with the cuff?

The BMC 2023 scoping review and several surgical series converge: between 36% and 93% of long head of biceps pathologies coexist with rotator cuff involvement, particularly of the subscapularis and supraspinatus.¹ ² The prospective Clin Orthop Relat Res 2025 study (n = 500 MRIs) confirms the linear LHB-cuff-age association.³ This almost systematic comorbidity has led several authors to reformulate the fundamental question: is the pain attributed to the LHB primary (the tendon's own involvement) or secondary (excessive loading in compensation for a failing cuff)?

This finding has major therapeutic implications :

• Isolated treatment of the biceps (stretching, self-massage, local injection) without correcting the cuff or scapular deficit is doomed to fail.
• The exercise programme must be centred on the cuff + the scapula, the biceps being only a secondary component.
• The initial assessment must systematically include cuff tests (Belly-press, Lift-off, Jobe, drop arm, external rotation lag sign).

How do you assess the overhead athlete: stratification strategy?

The overhead athlete (thrower, swimmer, tennis player, volleyball player, baseball player) presents a specific risk profile: a combination of repetitive overload, microtraumatic anterior instability, scapular dyskinesis and internal rotation deficit (GIRD). Cools 2015 (Braz J Phys Ther) proposes a structured 4-step approach for prevention and return to play:⁴

1. Identify risk factors : GIRD > 18°, total arc of motion deficit > 5°, visible scapular dyskinesis, external rotation weakness.
2. Establish normative criteria : ranges of motion, isokinetic strength, strength ratios (internal/external rotation).
3. Apply a prevention programme : posterior stretching (sleeper stretch), specific cuff + scapula strengthening, motor control.
4. Return-to-sport criteria : strength ≥ 90% of the contralateral side, IR/ER ratio ≥ 0.66, pain-free sport-specific plyometric tests.

Why do proximal rupture and distal rupture not have the same prognosis?

The two ends of the same muscle do not rupture for the same reasons or with the same consequences, and this is the first thing to establish in consultation.

The proximal rupture, at the shoulder, occurs on an already degenerative tendon: it is the culmination of the continuum described in chapter 1, often after a banal effort, and is accompanied by the classic “Popeye sign”. As the short head and the supinator partly compensate, the loss of strength remains modest and treatment is most often non-surgical, with tenotomy or tenodesis remaining debated in young patients bothered by cramps or deformity.

The distal rupture, at the elbow, is an entirely different lesion: an avulsion of the insertion on the radial tuberosity, under sudden eccentric load, with the elbow flexed at around 90°. It is rare: analysis of a large American insurance database estimates the national incidence at 2.55 per 100,000 patient-years (5.35 in the authors' local cohort) and affects a very homogeneous profile: mean age 46.3 years, 95% men nationally and 96% in the regional cohort. Smoking and a high BMI are associated with it; diabetes is not.¹ Here the ruptured tendon cannot compensate: it must be reattached to recover supination, and the window for doing so simply is measured in weeks.

How do you recognise a distal rupture at the elbow?

The diagnosis is clinical, and it is regularly missed. The hook test described by O'Driscoll is the reference manoeuvre: the patient actively supinates, elbow flexed at 90°, and the examiner tries to hook their index finger under the distal tendon from the lateral edge. An intact tendon lets the finger pass under a distinct cord; in a complete avulsion, there is nothing left to hook. In the original series of 45 patients, all surgically explored, the test was abnormal in 33 complete avulsions out of 33, intact in the 12 partial ruptures out of 12 (but painful in 9 of them) and normal in all 45 healthy contralateral arms. Sensitivity and specificity reach 100%, against 92% and 85% for MRI in the same series.²

Yet we must not be reassured by the appearance of the arm. The bicipital aponeurosis (lacertus fibrosus) remains intact in 59% of complete ruptures: it holds the muscle belly, limits retraction (the median biceps crease ratio goes from 2.2 when it is ruptured to 1.5 when it holds) and the contour of the arm may remain almost normal. The test dedicated to its integrity, described by ElMaraghy and Devereaux, reaches a sensitivity of 100%, a specificity of 90% and an overall accuracy of 94% in their cohort of 17 patients.⁴ The absence of visible deformity therefore does not rule out a complete rupture.

The practical approach follows from these figures: apply the three tests in sequence. Of 48 suspected patients, 35 had unequivocal results (all 32 concordant positives were confirmed intraoperatively), and sensitivity and specificity both reach 100% when the three agree, with no confirmatory imaging. It was the 13 patients with discordant tests who needed imaging to decide.³ In other words, MRI serves to arbitrate between contradictory examinations, not to validate a clear examination.

Should a distal rupture be operated on, and how quickly should the patient be referred?

The decision does not rest with the physiotherapist, but the timing of referral does, and that is where what matters most is decided.

The largest meta-analysis on the question (62 studies, 2,481 cases) gives repair the advantage on almost all measurable dimensions: + 25.7% of flexion strength, + 27.6% of supination strength, + 11.1% of flexion endurance and + 33.9% of supination endurance, with a DASH that is 7.8 points better and a MEPS 7.4 points higher.⁵ The caveat lies in the very structure of this literature: 2,402 operated cases against only 79 treated without surgery.

The picture becomes more nuanced as soon as one looks at what happens to non-operated patients. In a retrospective cohort of 488 respondents followed for a mean of 44 months, the secondary conversion rate to surgery is 36% with no difference between partial ruptures (34%) and complete ones (39%). Surgery significantly improved the QuickDASH only for complete ruptures (− 4.9 points), and the proportion of patients reaching an acceptable symptomatic state did not differ between the two approaches. The authors conclude that non-surgical treatment remains a reasonable first-line option, the majority of patients reaching an acceptable state.⁶

The delay, for its part, cannot be made up. In 373 patients operated in a single centre, the technique used follows directly from the time elapsed: direct repair at 16 days on average, high-flexion repair at 82 days, allograft reconstruction at 274 days; the point at which the three become equally probable lies between the 25^th and the 27^th week. The overall complication rate was 12%, dominated by nerve injuries (7%).⁷ And when presentation is already delayed (more than 21 days), direct repair remains preferable to reconstruction with semitendinosus autograft: comparable strength, range of motion and complications, but better PREE and MEPI scores after repair.⁸

What does the physiotherapist do after a distal repair?

This is where the literature is most disappointing, and it is better to tell the patient so than to promise an optimal protocol that does not exist. The most comprehensive systematic review of post-repair rehabilitation (50 studies, 1,577 patients) finds no significant difference between early mobilisation and immobilisation, neither in the re-rupture rate, nor in the DASH, nor in strength ratios. The type of immobilisation (splint, sling or hinged brace) makes no difference either. The authors stress the weakness of the evidence: risk of bias mostly poor to moderate, quality of evidence low to very low on GRADE.¹¹

The return-to-sport review (42 studies, 1,093 patients) points in the same direction while outlining a trend: 91.5% of patients return to sport, 85.2% at their previous level or above, at 6.3 months on average. The highest return rates are seen with immobilisation of at most two weeks, active mobility started early and strengthening begun at ten weeks or less; the authors speak of associated trends rather than of demonstrated differences.¹²

What these two reviews leave the clinician is simple: the timetable is negotiated with the surgeon, not in the literature, and the physiotherapist's energy is better spent elsewhere. In the reference randomised trial on surgical approaches, the four re-ruptures observed were all linked to non-adherence or to a new trauma in the early phase, unrelated to the fixation technique.⁹ Education in protecting the repair therefore weighs more heavily than the choice between two protocols that nothing distinguishes.

It remains to know what to monitor, and that depends on the surgical approach, information that appears in the operative report:

• Single incision : transient neurapraxias of the lateral antebrachial cutaneous nerve markedly more frequent (19 patients out of 47 versus 3 out of 43 with double incision in the randomised trial).⁹ Warning the patient that this paraesthesia of the lateral border of the forearm is expected and most often regresses avoids an unnecessary urgent consultation.
• Double incision : fewer injuries to this nerve, but the meta-analysis of 2,622 patients finds more heterotopic ossification and a higher reoperation rate, as well as slightly less flexion and pronation range.¹⁰
• Flexion strength in the long term : the only lasting functional difference in the randomised trial is a 10% advantage for double incision beyond one year (104% versus 94% of the healthy side); the ASES, DASH and PREE scores, for their part, do not differ at two years.⁹

How do you make the patient an active participant in their recovery through self-management?

Patient empowerment is a major predictor of therapeutic success. ¹ Three concrete pillars:

• Symptom monitoring : the patient learns to use pain as a signal. Practice benchmark: pain ≤ 4/10 during exercise, stable or decreasing within 24 h. Smith 2017 shows a small short-term benefit of exercises that allow pain (moderate certainty), not the validity of this threshold.²
• Load management (pacing) : avoid activity peaks,³ use a diary or an app, progress according to symptomatic response. The acute:chronic workload ratio (ACWR), which comes from team sports, is validated neither as an injury prevention tool nor as a return criterion.⁹ ¹⁰ ¹¹
• Autonomy in the exercise programme : the patient understands the “why” of each exercise and knows how to progress or regress according to their response. Simple programme, feasible at home, with functional goals.⁴

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

Return to sport (RTS) must be based on criteria and not on a fixed time frame.⁵ ⁶ Progression follows the rehabilitation continuum:

1. Pain control : isometrics in non-provocative positions (Rio 2015).⁷
2. Restoring load capacity : HSR (Heavy Slow Resistance, Kongsgaard/Beyer) on the cuff and biceps, up to 3-4 sets of 6-8 repetitions at 80% of 1-RM, 2-3 times/week for 12 weeks.⁸
3. Energy storage / release : progressive plyometrics: medicine-ball throws, ballistic push-ups, push-press.
4. Return to sport : sub-maximal specific movements, then controlled progression of volume and intensity.

Case 1: young volleyball player, isolated tendinopathy (Jaiswal 2024)

One case report published in 2024 (PMC11262752) documents the rehabilitation of a young volleyball player with proximal biceps tendinopathy. The protocol rested on four components: initial assessment and patient education, pain management and rest, kettlebell eccentric training intended to develop eccentric strength and promote tendon remodelling, and kinesiotaping aimed at pain relief and structural stability.¹ The authors conclude that this combination is effective and underline the value of a global rehabilitation strategy, adjusted to the specific needs of each athlete.

Case 2: the diagnostic challenge, suprascapular nerve entrapment

Reviews of series of suprascapular nerve neuropathies (Memon 2019, n = 87) show that these entrapments often present with anterolateral shoulder pain, sometimes associated with weakness of external rotation and infraspinatus atrophy. The diagnosis is regularly made late because the clinical biceps tests may be positive (referred sensitisation), leading to a therapeutic delay.² Further work-up includes nerve conduction EMG and an MRI looking for a paralabral cyst at the spinoglenoid notch. Treatment ranges from targeted rehabilitation to surgical decompression.

Case 3: Boileau's hourglass biceps and spontaneous rupture

The original series by Boileau (J Shoulder Elbow Surg 2004) described 21 patients with an “hourglass biceps”: a hypertrophic intra-articular tendon, trapped in the groove during arm elevation, causing pain and marked limitation.³ A dynamic intraoperative test reproduces the phenomenon. All but one case were associated with a rotator cuff tear. Treatment consists of tenotomy or tenodesis after resection of the hypertrophic intra-articular portion. The arthroscopic technique for identification and management was detailed by Xu 2022 (Arthroscopy Techniques, PMID 35782846).⁴

The spontaneous rupture of the LHB on chronic tendinopathy produces the famous “Popeye sign” (Pawar 2020, J Orthop Case Reports). The deformity is impressive but the functional consequences are modest after rehabilitation: loss of strength estimated at 8-20% in supination and elbow flexion, often compensated by the short head and the supinator.⁵ Conservative treatment is preferred in older, low-activity patients; tenodesis is discussed in young/active patients or those concerned about the cosmetic result.

When, and to which other healthcare professionals, should you refer?

Referral is not an admission of failure, it is a component of patient-centred care.

• General practitioner / sports physician : the hub of the coordinated pathway. Systematic referral if red flags (non-mechanical night pain, weight loss, fever, progressive neurological deficit; Finucane 2020).¹
• Rheumatologist : suspected rheumatoid arthritis, spondyloarthritis, polymyalgia rheumatica in the older patient.
• Orthopaedic surgeon : failure of conservative treatment at 12 weeks, subscapularis rupture, hourglass biceps, irreparable pulley lesion, symptomatic type II SLAP lesion in the young athlete.²
• Psychologist / CBT : predominant yellow flags (major kinesiophobia, catastrophising, depression); CBT combined with physiotherapy improves outcomes in chronic musculoskeletal pain.³
• Strength and conditioning coach / coach : optimise the return to the sporting movement, plan load progression and monitor tolerance session after session.

How do you measure outcomes and overcome barriers to implementation?

The PROMs are essential. For the shoulder, the validated and recommended tools are:

• DASH (Disabilities of Arm, Shoulder, Hand): 30 items, MCID ≈ 10 points.
• QuickDASH (short version, 11 items, MCID ≈ 8 points).
• ASES (American Shoulder and Elbow Surgeons): 100 points (pain 50 + function 50), MCID ≈ 12-17 points.
• SPADI (Shoulder Pain and Disability Index): 13 items, MCID ≈ 8-13 points.
• VAS / NPRS (pain, MCID ≈ 2 points).

The Goal Attainment Scaling (GAS) makes it possible to individualise goals (3-5 goals scored from -2 to +2) and to quantify attainment; its psychometric validity in rehabilitation was reconfirmed by Krasny-Pacini 2019.⁴

The barriers to implementing recommendations are well documented (Slade 2022, JOSPT): lack of time, low confidence, outdated clinician beliefs, lack of institutional support.⁵ Effective strategies:

1. Interactive continuing education : hands-on workshops > passive lectures.
2. Audit + feedback : analysis of one's actual practice, identification of gaps.
3. Local opinion leaders : “champions” within practices or networks.
4. Integrated tools : PROMs and GAS in the patient record software to reduce the administrative burden.