Hamstring Origin Tendinopathy
Like any tendon attachment in the body, the hamstring origin is prone to overuse and wear-and-tear. Unlike most tendons, the source of ongoing trouble – tendon compressive loading – is almost impossible to avoid in the proximal hamstring. Tendinopathy is non-inflammatory tissue wear or breakdown at the enthesis. It can occur due to tensile overload, but the expert consensus is that compressive loading between the tendon and bone is the main causative factor. This can be direct compression, such as sitting on a hard chair for the hamstring origin, lying on one’s side for the gluteal tendons, or kneeling for patellar tendinopathy. It can also be due to joint and muscular movements which place the (underside) tendon into a position where it is brought into closer contact with the bone. This occurs for the Achilles insertion during dorsiflexion, for the gluteus medius tendon when sitting cross-legged, and for the hamstring when the hip joint is flexed.
The lateral hamstring, the biceps femoris, forms a conjoint tendon with the medial semitendinosus. The conjoint tendon arises from the inferior, posterior & lower lateral facet of the ischial tuberosity. Further superiorly, the biceps femoris tendon is continuous with the superficial fibres of the sacrotuberous ligament. The semimembranosus attachment is somewhat more lateral than the conjoint tendon attachment. The sciatic nerve is closely related and passes just laterally to the hamstring origin.
Tendinopathy occurs due to areas of compression between the undersurface of the tendon & the bone interface. The biceps femoris & semimembranosus are the tendons most affected. At the cellular level, there will be increased cellularity, ground substance accumulation, collagen disorganization, & neurovascular ingrowth. Scanning may reveal localized bony oedema & insertional tendon clefts. There will sometimes be involvement of the ischiogluteal bursa. As with most tendinopathies, it is likely that chronic disease will make the hamstring origin prone to partial tearing or avulsion injuries. Proximal hamstring rupture is discussed at in a separate article - click here to view.
Like the majority of insertional tendinopathies, HOT is caused by excessive compression of the tendon against the bone. This occurs due to direct compression (sitting) or positions of hip flexion &/or adduction that approximate the undersurface of the tendon to the bone. The condition is associated with sports that involve excessive tensile or compressive loads in positions of hip flexion or adduction (including hockey, tennis, the football codes, lawn bowling, sprinting, hurdling, and dancing). Excessive stretching (e.g. during yoga or Pilates) may also be a causative factor. HOT may arise secondary to partial hamstring origin tear, or post-surgical repair for complete rupture.
More specifically, contributing factors may include training errors, poor running or walking gait, gluteal or hamstring muscle weakness, tightness in the hip flexors or hamstrings, excessive uphill running, postural factors including anterior pelvic tilt, restricted hip extension range, poor lumbopelvic control, over-stretching, and heavy weight training. Intrinsic factors include older age, increased BMI, certain metabolic conditions including diabetes, and hormonal factors. Along with other tendinopathies, HOT is common in perimenopausal women, as falling oestrogen levels have been shown to adversely affect tendon health. In middle-aged and older individuals, prolonged sitting or sitting on low or hard seats is the most common cause.
There is usually deep buttock soreness localised over the ischial tuberosity. There will often be associated aching into the hamstring, due to secondary muscle tension or sciatic nerve irritation. In chronic cases, sciatic-related symptoms may include paraesthesia in the posterior thigh. However, this is not common. The pain is often aggravated by walking, stretching, running, squatting, lunging and sitting. Hard chairs become very uncomfortable. The pain will often improve during activity when the tissues are warm, but be worse on cool-down. Post-activity exacerbation may last several hours to a few days. Sometimes pain initially improves but worsens toward the end of activity. Stiffness will sometimes be present in the morning or after rest.
Palpation findings are often reported to be inconclusive, however in my experience tenderness can usually be located laterally or posteriorly on the ischial tuberosity, some 1-2 cm proximal to the inferior aspect. Diagnosis is assisted through the use of provocative testing. This involves progressively loading the tendon in positions of increasing hip flexion (e.g. see Goom et al 2016).
Other causes of pain in this region may be lumbar spine or SIJ referral, lumbar radiculopathy, proximal hamstring tear, and piriformis syndrome. Less likely is hip joint referral.
Most tendon rehabilitation programmes will take between 3 to 6 months. A progressive loading approach is the key to effective management. The aim is to reduce pain and promote tissue healing. There will often be a fine balance between insufficient and excessive loading. The type and degree of load will depend on the stage of the condition and the response to exercise. Loading will usually commence in outer range to minimize compression, and gradually progress to inner range as symptoms improve and strength returns.
Other intervention strategies include:
- Education to ensure the patient minimizes activities that increase tendon compressive loading.
- Soft tissue techniques to release tight myofascial structures.
- Strengthening of synergists including the ‘core’, the gluteal muscles and sometimes the adductors.
- Neuromeningeal techniques if necessary to address neural tethering and restriction.
- When necessary, running technique modification/gait retraining.
- Correction of aberrant movement patterns and postures including anterior or lateral pelvic tilt.
- Postural re-education & exercises.
- Use of unloading cushions and positions for sitting.
- Kinetic chain strengthening and a gradual return to sport and work-specific activities.
Interesting case history
‘Fiona’ had a one-year history of left SIJ / buttock and upper thigh pain. At times this extended into the lateral hip. The pain was aggravated by bending, particularly over the left hip. It was also aggravated by sitting, especially on hard or low chairs, or in the car. The lateral hip pain was aggravated by stairs, driving, and lying on either side at night. She saw a physiotherapist who prescribed flexion stretches and used lumbar traction. The stretches aggravated her pain. She was then referred to a neurosurgeon and subsequently for lumbar MRI. A previous X-ray & MRI revealed a Grade I spondylolisthesis at L5/S1, associated with disc degeneration and circumferential bulging. This resulted in encroachment on the nerve roots bilaterally. The neurosurgeon recommended L5/S1 fusion.
I saw Fiona soon after this. While she had a history of intermittent low back pain, this was not impacting on her daily life to any significant degree. The symptoms she described to me did not suggest lumbar spine referral. The pain was aggravated by direct compressive loading and deep hip bending. In addition, her pain was reproduced by palpation over the postero-lateral ischial tuberosity, and by resisted hamstring contraction with the hip flexed. She also had some tenderness of her gluteus medius insertion at the greater trochanter. I considered her pain to be due to hamstring origin tendinopathy, with mild gluteal tendinopathy. Fiona was peri-menopausal, and had a job that involved prolonged sitting. She also did a lot of driving. All of these factors were influencing her condition.
Treatment consisted of soft-tissue releases through the hamstring and posterior hip, and strengthening commencing with inner range isometric hip extension exercises. I recommended alterations to her seat including use of a wedge cushion at work and a dimple cushion for the car. On her second visit, I progressed her hip extension strengthening to short-range isotonic exercises, and these have been progressed further at each visit.
I saw Fiona on 5 occasions between June and August. She noticed an immediate improvement with her modified sitting, and continued to improve on each occasion. On her last visit, she reported being 95% recovered. She really only noticed the pain now if sitting on a hard surface. She could get around this by always having a portable dimple cushion with her.
Fiona still gets intermittent low back pain but manages this well. And the pain has not worsened over the past few years. The findings on imaging were incidental, and this case demonstrated the pitfalls in basing diagnosis purely on imaging findings, rather than a thorough and informed clinical examination.
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