Hamstring injuries can be one of the most debilitating and frustrating of all muscle injuries for athletes involved in sports requiring top-end speed. The difficulty with managing hamstrings is particularly evident in minor ‘Grade 1’-type strains. Is it true muscle pathology or is it a ‘neural hamstring’ mimicking muscle pathology? Differentiating the cause of posterior thigh pain can be an overwhelming clinical challenge. Furthermore, there is a wide practical gap between clinical treatment and a full return of the athlete to sport. In short, therapists must ask themselves, first, are they treating the right thing, and second, are they letting the athletes come back too early? To put this into perspective, recent statistical studies in Australia on injury types and injury frequencies have shown that 25% of hamstring injuries will recur in the first four weeks. To the optimist, this means that 75% of hamstrings you think are right to return to sport will do well. To the pessimist, this means that there is a 25% chance of re-injury and going back to square one.
This article and the next will focus on the practical rehabilitation of hamstring injuries. The third in the series will deal with groin injuries, and the fourth and final article will cover quadriceps injuries.
It is beyond the scope of this article to discuss all the presenting signs and symptoms of the above differentials. Instead, it will concentrate on the differentiation between true muscle injuries and ‘neural hamstring’ problems.
Hamstring pain or ‘posterior thigh’ pain can present in many different ways. On one end of the spectrum, we have true tears involving local muscle pathology. These are usually sudden onset and involve a definite grabbing or tearing sensation with associated moderate to severe pain. Strong Grade 2 and Grade 3 strains will be functionally limiting, with walking often painful. The grading nomenclature is well covered in most sports medicine textbooks, and I am assuming that most SIB readers will be familiar with these.
Acute ‘cramping’ or ‘spasm’ of the hamstring may also cause sudden onsets of pain. These are commonly referred to as ‘neural hamstrings’. That is, an increase in hamstring tone is the cause of the cramping pain. However, the causative factors for the increase in muscle tone are very often much more difficult to determine. The tone increase may be a response to referred pain from the lumbar spine, sacroiliac joint, neuromeningeal structures or local myofascial trigger points.
Patients who present with ‘niggling’ recurrent cramping, spasm and minor aches and pains may appear to have minor Grade 1 strains. However, although these types of neural hamstrings are not limited in performance other than top-end speed, they are often the more frustrating and difficult to manage. They are the ones who never miss a game, but are never at 100% either. A better understanding of referred pain, lumbar spine involvement and neuromeningeal dynamics will help differentiate true muscle pathology from ‘neural hamstrings’.
The most common mechanism of injury for hamstrings is during acceleration or rapid deceleration. Under these conditions, the muscle is subjected to the greatest amount of eccentric force. High-speed athletes tend to suffer hamstring problems in the cross-over from eccentric deceleration of the swinging leg prior to foot strike, to the rapid concentric contraction required at foot strike into pull-through hip extension. The degree of failure of the musculo-tendinous unit can vary from complete disruption (Grade 3) to non-disruptive strain (Grade 1-2). The biceps femoris is the most commonly involved hamstring in ‘true’ muscle tears. It has been postulated that the biceps is more injury prone due to the dual-nerve innervation of the short and long head. It is proposed that poor coordination, especially under fatigue, of the two heads predisposes the biceps femoris to muscle tears.
The location of ‘neural’ hamstrings, on the other hand, are much more difficult to pinpoint. They will be commonly felt in the medial muscle bellies, or between the semimembranosis and biceps femoris, or the sensation may move around the muscle from episode to episode. The clinician will usually identify concurrent increased tone in muscles further north of the hamstring, e.g.: gluteus medius, TFL, psoas, quadratus lumborum.
Hamstring injuries are not restricted to running. Other common mechanisms of injury are kicking (especially long kicking), sudden side stepping, overstretch when caught in an awkward position and landing in knee hyperextension from a jump.
Two schools of thought exist here regarding the underlying cause and effect relationship of true ‘muscle’ hamstring injuries. First, under all of the above circumstances the assumption is that the force applied to the muscle exceeds the tensile properties of the muscle. The muscle is stretched too much or contracts too hard and reaches breaking point. Secondly, practitioners from a ‘myofascial’ background will argue that increased tone will exist first and cause the muscle to be already pre-strained. Overstretch/contraction simply pushed the pre-strained muscle to tearing. Without pre-existing tone in the muscle the hamstring should not tear under normal circumstances.
Both ‘muscle’ hamstrings and ‘neural’ hamstrings may exhibit weakness and pain on strength testing. One distinguishing clinical feature is that if the hamstring is weak but not painful, then the problem is more than likely a neural hamstring. Muscle injuries more often than not present with weakness AND pain on contraction, irrespective of the grade of the tear. However, a neural hamstring with no local muscle involvement may still be painful on testing and on palpation due to peripheral sensitisation.
Pain, inhibition and weakness with a true muscle tear are a result of the pulling of the disrupted fibres. Weakness and inhibition with a neural hamstring may be caused by nerve root compression, active myofascial trigger points in the gluteals and/or hamstrings or pain inhibition caused by a lumbar disc problem.
A number of useful strength tests exist to help the diagnosis of injury, evaluating response to treatment and determining progression and recovery.
The patient lies on his/her back, with their heel on the therapist’s shoulder (sitting on bed/plinth at their feet). The patient pushes down onto the therapist’s shoulder while attempting to lift their body off the bed (pivoting of their own shoulders). Gauge ability to contract and lift body, and pain response. This is done, first, with hip at 30-45 degrees and knee fully extended, then with knee bent to 45 degrees, and finally hip and knee bent to 90 degrees.
Performing the functional bridging test allows the therapist to assess the strength of the hamstring in a functional way (as it involves hip extension as well as knee flexion), but also to assess varying points in range. It is difficult to directly correlate the specific bellies of the muscle with these tests. What they do well is to allow a re-assessment point for future progression and response to treatment.
A version of the traditional prone-resisted knee flexion. This can be done with different positions of tibial rotation to target the medial and lateral bellies of the hamstring. This test allows us to gauge a side-to-side difference in strength and pinpoint areas of pain. An effective extension of this test is to load up the eccentric component of the test with a quick eccentric load, particularly towards the end of range. This will show up continuing weakness in the hamstring at late stages. Not recommended in a fresh injury due to the rapid and large eccentric loads.
Decreased range of motion will be present in both ‘true’ hamstring pathologies and ‘neural’ pathologies. A number of clinical tests exist to give the clinician an objective measure of hamstring range of motion. The two range tests are Straight Leg Raise (SLR) and Passive Knee Extension (PKE) or ‘Bowstring’ stretches.
Similarly with the strength tests, the range tests give the clinician a point of reference in determining the effects of treatment and the rate of progression of the pathology.
It is important with all these tests to gain an impression of the initial point in resistance (or the R1) and the end point in resistance (R2). From a functional point of view, the R1 is of greater importance. As the muscle reaches its R1 during movement, compensatory mechanisms in adjacent joints (eg, lumbar spine) will begin. It is not uncommon to feel a straight leg raise with an R2 of 100 degrees (which may be considered impressive); however, with an R1 starting at 50 degrees. In this instance, when the hip reaches 50 degrees of movement (such as kicking) then the pelvis will start to posteriorly tilt and lumbar spine begin to flex a long way before the hamstring reaches its 100 degrees of R2. This is important to consider when using range of motion measures to understand the way joints function as part of a kinetic chain.
Performed by passively raising the leg with the knee in extension. It is important to keep the pelvis neutral and watch and feel for any compensatory posterior pelvic tilt. This test will put the muscle, nervous system and fascia on stretch. It is therefore important to differentiate muscle from the nervous system by adding in a sensitising movement such as dorsiflexion of the ankle at end range. If the nervous system is the source of pain, dorsiflexion will reproduce the exact pain and there will be a difference compared with the unaffected side.
To make things interesting, recent anatomical studies released in Holland by Andre Vleeming & Chris Snijders suggest that the fascia covering and blending with muscle is more extensive and continuous than previously appreciated. Therefore, a SLR with dorsiflexion may actually be eliciting a response in the fascial system, not the neural system, as this manoeuvre will also strain the posterior calf fascia that blends with the fascia lata in the thigh, which blends with the thoracolumbar fascia in the lumbar spine.
With the hip held passively at 90 degrees, the knee is passively extended to gain a measurement of the R1 and R2, pain response and side-to-side difference. The benefits of this test are that, first, the pelvis is held fixed through the test and does not contribute to the measure of range and that, second, this test places an emphasis on the functional way the hamstring works in running (i.e., knee extension while in hip flexion). Finally, it has been proposed that the bowstring stretch loads and strains a different part of the hamstring to a SLR. This explains why some acute hamstring tears can be pain-free with a SLR but painful on a bowstring.
Neuromeningeal dynamics describes the contribution the nervous system makes in terms of its movements over and against interfaces such as discs, joints, fascial tunnels, muscles and bone. The contribution that the sciatic nerve makes in hamstring pathologies has been documented elsewhere and will not be mentioned here.
Testing the dynamics of the nervous system can be done in two ways. First, using a SLR as mentioned above with dorsiflexion to test the tibial portion of the sciatic nerve, or SLR with plantar flexion and inversion to add in the superficial peroneal nerve. This is more significant in biceps femoris injuries. Second, execution of a SLUMP test can assist in differentiating hamstring vs. neural and/or fascia. For those unfamiliar with this test, it involves sitting on a plinth, hands behind the back, actively extending the knee and then flexing the cervical spine and then the trunk. Pain in the posterior thigh can be differentiated by extending the cervical spine or adding plantar flexion of the ankle and then assessing the pain response as originating from the muscle or nerve. Again, caution must be taken with the contribution of the fascial coverings extending from the cervical spine, continuing with the thoracolumbar fascia, into the biceps femoris and fascia lata of the thigh.
It is beyond the scope of this article to go into detail on the role that the lumbar spine plays in hamstring pathology. Poor mobility in and between lumbar spine joints, and poor linking between the lumbar spine and the pelvis can place unnecessary stress on the musculature of the thigh, hamstrings in particular. Furthermore, specific lumbar spine pathologies can refer pain into the posterior thigh or interfere with the proper functioning of the central nervous system and the sciatic nerve.
What is interesting to note is the sudden and dramatic improvement that some ‘neural hamstrings’ enjoy following lumbar spine and caudal epidural cortisone injections. Local inflammation on the spinal cord and nerve roots can and will place the sciatic nerve in an irritable state. This can in turn lead to altered motor output from the nerve and associated reactive spasm in the hamstrings. By reducing the inflammatory component, the nerve may better function and as a result the hamstring will react less to the irritant. This is the rationale behind an invasive procedure such as an epidural cortisone. However, it is still important to determine the cause of the inflammatory state in the first place. It is not a good idea for an athlete to be having epidurals every 2-3 months to continually settle a hamstring problem as it represents an adjunct to the rehabilitation process.
Controlling movement of the lumbar spine and pelvis is an essential component in providing a solid base from which the thigh muscles can function. Good activation and patterning of the deep stabilising muscles and the superficial ‘core’ muscles will reduce stress on the spine and minimise unwanted transfer of stress to the thigh muscles.
Similarly with abdominal control, assessing and maintaining muscle tone around the musculature around the pelvis will assist in normal pelvic biomechanics. This is a complex area that warrants more detail than we have room for here; however, the reader is directed to any material on muscle energy techniques to further understand dealing with this somewhat difficult area.