Proximal Hamstring Tendinopathy: A Challenge for Athletes and Clinicians

Tendon injuries are a common sporting problem. Whilst much attention is focused on the more common issues of Achilles and patella tendon pain, proximal hamstring tendinopathy (PHT) is a condition that, if inappropriately managed, can lead to persistent performance decrements in the first instance and thereafter extended time loss. Sports such as the various football codes played around the world, provide the perfect combination of injurious mechanisms, with relatively high running distances and velocities, alongside a kicking technique which can lead to a long ‘shank arm’ adding further load to the region.

Anatomy

The hamstrings are a biarticular muscle group consisting of the bicep femoris (BF), semimembranosus (SM) and semitendinosus (ST). The ST and the long head of BF unite to form a conjoined tendon before attaching to the posteromedial portion of the ischial tuberosity. The SM is considered to have a deeper attachment, originating just anterolaterally to the conjoined attachment on the ischial tuberosity.

It is important to note that the proximal tendon has an intimate relationship with the inferior gluteal nerve, artery, and the sciatic nerve, this often means that PHT is accompanied by a neural irritation. An appreciation of the local structures is required to assist clinicians in making differential diagnosis.

The hamstring muscles work isometrically to maintain standing posture, resisting excessive postural forward lean and excessive lumbar lordosis. When we consider the lever arm of the hamstrings in relation to the hip joint, it becomes significantly larger or smaller as the hip joint changes position. Consequently, the hamstrings will be required to work in situations where there is forward flexion in the hip or trunk, with the proximal hamstring tendon and its attachment to the ischial tuberosity subjected to higher loads when placed in this position⁽¹⁾. In running, during terminal swing phase, the hamstrings are required to rapidly decelerate knee extension. Energy storage in the late-swing/early-stance stretch-shorten cycle is thought to be a potential risk factor for PHT.

Aetiology

Cook and Purdam presented a model describing the progression of a tendon from normal to pathological⁽²⁾. In this model, a tendon can adversely react to imposed load by increasing tenocyte activity and protein synthesis. At this stage with appropriate load modification, the tendon heals well. However, should load exceed tolerance, the tendon’s collagen structural framework can be disrupted.

Whilst there is limited research on PHT, it is thought that the pathological presentation is similar to findings in the other weight-bearing tendinopathies⁽³⁾. From the limited studies available, PHT presents with localised tendon pathology at the enthesis, bone oedema and insertional tendon clefts^(3-5).

In the athletic population tendinopathy represents a maladaptive response to an increase in load. The extrinsic risk factor of a causative spike in training load over days or weeks, coupled with intrinsic biomechanical and movement pattern dysfunctions, leads to deterioration in the tendon health. Other extrinsic risk factors that require consideration include:

• An injury to another tissue or structure above or below the chain
• A change in footwear
• A change in terrain
• A change in external resistance

The clinician is also encouraged to review the intrinsic risk factors related to tendinopathy. It is thought intrinsic risk factors reduce the threshold for tendon pain and pathology. These include; age, body mass index, metabolic issues, hormonal change, and fluoroquinolone antibiotic use (see Sports Injury Bulletin issue 153 for an in-depth discussion of fluoroquinolones in sport).

Subjective assessment

Often the athlete will report a gradual insidious onset of localised deep buttock pain and tightness over the ischial tuberosity and gluteal fold region. Running at higher velocities is often implicated as an aggravating factor, but like many tendinopathies it will often ease following a thorough warm-up.

As the condition deteriorates, the pain fails to settle, limiting top end pace and worsens with increased duration of running volume or repeated provocative movements. A thorough history may reveal the positions of provocation place the proximal hamstring tendon under compressive load at the ischial tuberosity, such as the dead lift, squat, lunge, high step up and repeated kicking out of hand. Moreover, periods of prolonged sitting increase compression and can aggravate symptoms. As such, it is not just training loads that need to be fully understood but also sitting loads. It is unsurprising therefore that this condition is often seen in athletes that are also studying or have high driving mileage.

Whilst completing the subjective assessment it is important to listen to the way the athlete describes their pain and their relationship to pain. An understanding of the psychosocial influencers of pain in PHT will dramatically improve a clinician’s chances of engagement if detrimental beliefs are held by an athlete.

Fear avoidance, anxiety and a heightened attention to PHT may lead to amplification of neural signalling within the central nervous system that then elicits pain hypersensitivity^(6,7). This effect has been found in other tendinopathies⁽⁸⁾, and if not addressed can dramatically affect recovery. The reader is encouraged to read the work of Woolf, addressing central sensitisation⁽⁷⁾.

Differential diagnosis

It has been observed that PHT cases in athletes are often associated with a past medical history of hamstring strains and/or sciatic nerve compromise. It is not uncommon in more chronic cases for supposed isolated hamstring strains to coexist⁽³⁾. Once a detailed subjective history has been established, the clinician must consider the other structures that may present in an analogous way. Utilising a systematic approach to inclusion/exclusion will ensure all appropriate co-morbidities and differential diagnoses have been accounted for (see Table 1).

*Adapted from Caine 2017⁽⁹⁾

Imaging

Most often, the diagnosis of PHT can be made without radiographic imaging, but it can be helpful to rule out other structures that may be implicated in the dysfunction. magnetic resonance imaging (MRI) is the gold-standard technique and PHT commonly presents with thickening and surrounding oedema, along with changes mimicking bone marrow oedema, which show this is more an isolated tendon issue.

However, what is worthwhile noting are the findings of a recent study showing these same signal changes are found in asymptomatic patients just as readily as symptomatic cases⁽⁴⁾. The importance of treating the individual based on the clinical presentation and not just the reported findings must be at the forefront of a clinicians mind - i.e. ‘treat the man not the scan’!

Objective

Whilst validated tests for PHT with high sensitivity and specificity are limited, three passive stretch tests (bent-knee stretch, modified bent-knee stretch and the Puranen-Orava test) have moderate to high validity and high sensitivity⁽¹⁰⁾. A test is positive when proximal hamstring pain is elicited with compression on the ischial tuberosity. However, these tests have been found to be less sensitive for early/less symptomatic PHT presentations.

The author uses a straight-leg variant ‘raging bull test’ in a hip flexed position. The athlete is asked to isometrically pull their heel down and back into the floor for a few seconds; pain provocation during or immediately on release can indicate PHT. The pain provocation test continuum looks to place the tendon under progressive compression and tensile load by increasing hip flexion angles. Tests are initially completed slowly, tempo is accelerated if asymptomatic at slower pace. The pain score should increase with load across these tests.

PHT pain provocation tests (Figure 1)

A: Short level bridge (low-load test) - upper left
B: Long lever bridge (moderate load test) - bottom left
C: ‘Raging bull’ pull variant (moderate-high load test) - upper right
D: Arabesque (high load) - middle right
E: Single leg dead lift (high external load test) (Cook, 2014). - bottom right