Lumbar spine region pathology and hamstring and calf injuries in athletes – is there a connection?

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The Australian Football League (AFL) injury survey, over more than a decade, has shown that common lower limb soft-tissue injuries that involve L5 and S1 nerve supply have a marked correlation with increasing player age [1, 2] . However, similar injuries involving L2-L4 nerve supply are not related to player age [1, 2] . Table 1 shows how dramatic this bias is:

Table 1 – Injury prevalence (missed games per team per season) by player age, Australian Football League (reprinted with permission from Sport Health)

It is presumed that muscles and tendons are more susceptible to injury as they age, but it not clear why injuries to soft tissues with a L5 and S1 nerve supply have such a strong correlation with advancing age, whereas there is little or no correlation between age and the soft tissue injuries with a L2-L4 nerve supply.

Many clinicians subscribe to the concept of a ‘back-related’ hamstring injury (or more specifically lumbar spine-related) [3-5] although this is a controversial paradigm to researchers as no specific mechanism has ever been proven for such an injury. The lumbar spine-related hamstring is considered to be an injury that presents clinically as a hamstring strain (usually with a more gradual onset) but is MRI-negative. As the resolution of MRI scan improves, a greater proportion of posterior thigh injuries are proven by MRI to actually be hamstring muscle strains, although some suspected hamstring injuries still turn out to be MRI-negative [3] .

Many clinicians also believe that athletes with lumbar spine pathology have a greater predisposition to hamstring strains, although this has not been prospectively proven. A recent study by Verrall et al. showed that football players with a past history of lumbar spine injury had a higher rate of MRI-negative posterior thigh injury, but not of actual hamstring strain [3] . In a clinical setting, piriformis syndrome [6] has been occasionally suspected of causing recurrent hamstring pain in athletes. Theoretically, any pathology relating to the lumbar spine, the lumbosacral nerve roots or plexus or the sciatic nerve could result in hamstring or calf pain (amongst other symptoms).

It is known that back injuries are very common in elite athletes, particularly at the L5/S1 level [7] . Figure 1, from a study by Ong et al., shows a bias towards lumbar degenerative changes occurring at L4/5 and L5/S1 levels, compared to the more proximal levels [7] . The cohort in this study was 31 Olympic athletes aged from 19-46, with two-thirds in the 20-30 year age group. It is tempting to draw an association between the correlations with the findings related to L5 and S1 levels in Table 1 and Figure 1.

Figure 1 – Reproduced from British Journal of Sports Medicine [7] .

It is easy to appreciate that an acute disc prolapse at L5/S1 level may present with hamstring and/or calf pain and limitations in flexibility which may mimic a muscle strain. There is a further mechanism by which less acute L5/S1 pathology may potentially lead to symptoms (or possibly even strains) in the hamstring and calf muscles. Of all of the nerve roots in the lumbosacral plexus, the L5 has the most tortured path through the lumbosacral canal and over the anterior superior ridge of the sacrum, after which it joins the sacral plexus. Briggs et al. dissected the lumbosacral ligament (an inconsistent extension of the iliolumbar ligament) in the pelvis, and showed a correlation in cadavers between L5/S1 degenerative changes and compression of the L5 nerve root by the lumbosacral ligament [8] . The cadavers were aged between 60 and 90 years but varied in the relationship of lumbosacral ligament to the nerve, with 9% showing nerve compression and visible flattening of the L5 nerve root by the ligament [8] . The lumbosacral ligament and its propensity for extraforaminal entrapment of the L5 nerve root was first described by Nathan et al. [9] and by other anatomists since [10, 11] , with extraforaminal entrapment of L5 nerve root actually first described in 1925 [12] .

The lumbosacral ligament, which is present to a degree in all individuals [9, 13] , is visible on MRI scans in certain ‘normal’ patients (using T1 axial scan on a 1.5 Tesla scanner) (Figure 2) and not in others. It is difficult to assess whether this is because the ligament is atrophic or actually absent in some patients or because the resolution of 1.5 Tesla scans is not great enough to properly assess the ligament in all patients. The study of Briggs et al., whilst involving cadavers whose average age was much greater than that of the average athlete, suggests that the lumbosacral ligament may develop or hypertrophy in response to degenerative changes of the L5/S1 region.

Figure 2 – Lumbosacral ligament (marked by four large red dots) and its relation to L5 nerve root (marked by three small yellow dots) at the level of L5/S1 disc (T1 axial view).  

It is possible that the anatomical configuration of a hypertrophied lumbosacral ligament is more clinically significant in older athletes with the common finding of L5/S1 degenerative disc changes. Perhaps, via subtle L5 nerve root entrapment, it is a factor in some of those players who find that they have recurrent hamstring and calf musculo-tendinous injuries despite regular preventive maintenance. This hypothesis is interesting as it provides potential additional treatment options to the athlete with recurrent hamstring, calf and Achilles injuries, which are common in all football codes, track and field, racquet sports and cricket.

To date we have already had positive experience (although not in the perspective of a controlled study) with imaging-guided cortisone injections to the lumbosacral canal region (L5 nerve root) in athletes with peripheral symptoms, such as recurrent hamstring and calf pain. This is a relatively painless and complication-free outpatient procedure with quick recovery. We have used this both for acute symptoms and as a preventive procedure in highly susceptible athletes (with a history of multiple muscle strains and pathological changes in the lumbar spine). The limitation from cortisone injections is that any relief from subtle nerve entrapment is only likely to be short-term in the majority of cases.

Unfortunately, the lumbosacral ligament is not easily accessible for surgical treatment. The best method for reaching it would probably be through an anterior approach with an abdominal laparoscope. This approach would be a posterolateral abdominal incision anterior to quadratus lumborum. The lumbosacral canal is found between the iliac vessels and psoas. This type of surgery has recently been described by Matsumato et al. [14] . A posterior approach would be technically easier, but would involve far more surgical trauma of muscles and probably bone (the sacral ala).

It remains to be seen whether it would be technically easy to divide the ligament to free an entrapped L5 nerve root, and whether this procedure would reduce the risk of hamstring or calf injury in a susceptible athlete without causing side effects. There are major possible complications of surgery including potential for damage to the iliac vessels and L5 nerve root itself and potential for L5/S1 segment instability (if the lumbosacral ligament develops as a critical stabilizer of the L5 vertebrae).

Proving the diagnosis of subtle extraforaminal L5 nerve entrapment, using non-invasive methods, remains problematic. Whilst MRI scan resolution improves all the time, it can currently isolate structures in the region that may possibly cause entrapment (such as a thick band of the lumbosacral ligament) but probably cannot demonstrate the signs of a nerve entrapment in this region, such as a thinning of the nerve diameter as it passes underneath the ligament. Neurodiagnostic tests may potentially be helpful but EMG and nerve conduction changes may only be present post-exercise, and even if positive, would have great difficulty at distinguishing between entrapment at the neural foramen, in the lumbosacral canal or by tight muscles in the gluteal region.

It is most plausible that extraforaminal L5 nerve root entrapment is one of many explanations for a propensity to hamstring and calf symptoms in athletes, in a fashion that is analogous to piriformis syndrome [6] , sciatic nerve entrapment by the internal obturator muscle [15] and hamstring syndrome [16] . Perhaps multiple subtle entrapments can be present at the same time and be additive, leading to motor dysfunction of the hamstring and calf muscle groups. In a similar fashion to those other previously described syndromes, we believe that the anatomical configuration of lumbosacral ligament entrapment of the L5 nerve root has significant potential to help explain the pathogenesis of posterior thigh and calf injuries in certain athletes. Whilst this configuration has been well described in the neurological literature for many years, it may also be relevant in the field of sports medicine.

References:

1.         Orchard J ,Seward H. AFL Injury Report 2002. Sport Health 2003; 21(2): 18-23.

2.         Orchard J. Intrinsic and extrinsic risk factors for muscle strains in Australian footballers. Am J Sports Med 2001: 300-303.

3.         Verrall G, Slavotinek J, Barnes P, Fon G, Spriggins A. Clinical risk factors for hamstring muscle strain injury: a prospective study with correlation of injury by magnetic resonance imaging. Br J Sports Med 2001; 35: 435-440.

4.         Orchard J, Marsden J, Lord S, Garlick D. Preseason hamstring muscle weakness associated with hamstring muscle injury in Australian footballers. Am J Sports Med 1997; 25(1): 81-5.

5.         Bennell K, Wajswelner H, Lew P, Schall-Riaucour A, Leslie S, Plant D, Cirone J. Isokinetic strength testing does not predict hamstring injury in Australian Rules footballers. Br J Sports Med 1998; 32(4): 309-14.

6.         Pecina M, Krmpotic-Nemanic J, Markiewitz A. Piriformis muscle syndrome, in Tunnel syndromes. Peripheral nerve compression syndromes. 1997, CRC Press: Boca Raton . p. 185-192.

7.         Ong A, Anderson J, Roche J. A pilot study of the prevalence of lumbar disc degeneration in elite athletes with lower back pain at the Sydney 2000 Olympic Games. Br J Sports Med 2003; 37: 263-266.

8.         Briggs C ,Chandraraj S. Variations in the lumbosacral ligament and associated changes in the lumbosacral region resulting in compression of the fifth dorsal root ganglion and spinal nerve. Clinical Anatomy 1995; 8: 339-346.

9.         Nathan H, Weizenbluth M, Halperin N. The lumbosacral ligament (LSL), with special emphasis on the "lumbosacral tunnel" and the entrapment of the 5th lumbar nerve. Int Orthop 1982; 6: 197-202.

10.       Transfeldt E, Robertson D, Bradford D. Ligaments of the lumbosacral spine and their role in possible extraforaminal spinal nerve entrapment and tethering. J Spinal Disord 1993; 6: 507-512.

11.       Olsewski J, Simmons E, Kallen F, Mendel F. Evidence from cadavers suggestive of entrapment of fifth lumbar spinal nerves by lumbosacral ligaments. Spine 1991; 16: 336-47.

12.       Danforth M ,Wilson P. The anatomy of the lumbo-sacral region in relation to sciatic pain. J Bone Joint Surg 1925; 7: 109-160.

13.       Pecina M, Krmpotic-Nemanic J, Markiewitz A. Lumbosacral tunnel syndrome, in Tunnel syndromes. Peripheral nerve compression syndromes. 1997, CRC Press: Boca Raton . p. 165-167.

14.       Matsumoto M, Chiba K, Nojiri K, Ishikawa M, Toyama Y, Nishikawa Y. Extraforaminal entrapment of the fifth lumar spinal nerve by osteophytes of the lumbosacral spine: anatomic study and a report of four cases. Spine 2002; 27: E169-73.

15.       Meknas K, Christensen A, Johansen O. The internal obturator muscle may cause sciatic pain. Pain 2003; 104: 375-380.

16.       Orava S. Hamstring syndrome. Operative techniques in sports medicine 1997; 5(3): 143-149.

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