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Nerve entrapment syndrome

Nerve entrapment syndrome: Leg pain in athletes

The Sports Injury Doctor

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An overview of common sports-related injuries, focusing on nerve entrapment syndromes. By Shahid Punwar, Fares Haddad and Chris Bradshaw

Exercise-induced leg pain is common, with numerous known causes. It is often multifactorial, and its source may be local or distant from the site of pain. Once musculoskeletal causes, compartment syndrome and vascular compromise have been excluded from a diagnosis, nerve entrapment syndromes should be considered as a possible cause of symptoms. This review summarises the main causes of sports-related leg pain and then looks in more detail at those where nerve entrapment is a factor.

Leg pain: non-neural pathologies

Shin splints

This term tends to cover many disorders that cause exercise induced leg pain. Initially ‘shin splints’ was thought to be caused by tibialis posterior tendon injury. Other ‘overuse’ conditions, including compartment syndrome, tibialis anterior strain, tibial periostitis and tibial stress fracture have all indiscriminately been referred to as ‘shin splints’. Given the very different pathologies of these conditions, the term is not really very useful. Instead, the therapist should identify and address the specific condition being presented.

Muscle strain

Muscle fibres may be damaged by over-stretching; the most likely site being tibialis anterior at the front of the shin. Symptoms are acute pain within the muscle at the site of the tear, during contraction and stretching. The area may also be swollen and warm. Once swelling has subsided, treatment should focus on stretching and strengthening the affected muscle within the limits of pain.

Tendinopathy

This is where microtears in a tendon cause inflammation in the surrounding tissue. It is an overuse injury, generally caused by excessive repetitive movements, particularly over-stretching and eccentric loading of a muscle. In the leg, the most likely site is tibialis posterior, possibly as a result of repeated hyperpronation.

Symptoms include pain, swelling and a palpable crepitus (crunchy feeling) along the tendon during muscle contraction. Pain occurs mainly at the start of and after exercise. In the initial stages of treatment, painful activities should be minimised and the client should take regular anti-inflammatories. Complete rest is not advised, as tendons heal better when given mild, normal loading. Once inflammation and pain have subsided, the muscle of the affected tendon should be stretched and strengthened.

Medial tibial stress syndrome (MTSS, periostitis)

Bone bending is a natural consequence of weight bearing. Wider bones resist bending better than narrower ones and are therefore less prone to injury. Chronic repetitive bending stimulates a long bone to widen its cross section by activating bone cells in its periosteum (outer layer) to lay down new bone. If increases in training intensity continue to occur during the process of adaptation, the bone cells cannot keep up and the region becomes inflamed. The injury may be compounded by simultaneous repetitive muscle pulls on the periosteum.

The area most affected is the lower half of the medial tibia, where the bony cross section is narrowest. Symptoms and signs are pain during weight bearing (particularly running), and tenderness to the touch. Sometimes there is also swelling, redness and warmth. Treatment is full rest from painful activities with a very gradual return to training. Muscles should not be stretched or strengthened while symptomatic.

Tibial stress fracture

These are incomplete cracks in the tibia where repetitive loading has overcome the ability of the bone to resist it. They may occur more frequently in specific sports such as long-distance runners. Once diagnosed a period of complete rest (15 days minimum) from painful weight-bearing activity is crucial. Although uncommon, spontaneous complete fractures may occur if the advice to rest is ignored. Typically stress fractures will heal in four to eight weeks, though lesions on the anterior (front) border of the bone may take many months to heal and may require electrical stimulation or grafting. It is not uncommon for tibial stress fractures to recur.

Chronic exertional compartment syndrome

This overuse condition, caused by tight fascia around the muscles, produces symptoms during and for about 15 minutes after training. Typical post-exercise examination findings include tightness in the rear lower leg compartments and paraesthesia (pins and needles). The diagnosis can be confirmed by pressure testing after exercise. Pain is often described as cramping. There may also be muscle tears. Some sports physicians advocate elective fasciotomy to release the fascia and reduce the pressure(1). Chronic exertional compartment syndrome should not be confused with acute compartment syndrome – a medical emergency which can occur after a direct blow to the lower leg.

Popliteal artery entrapment syndrome

This uncommon pathology may be found among young sportspeople who present with ischaemic (restricted blood supply) symptoms in the lower leg, including pain, pallor and paraesthesia. It is related to the intensity of exercise and drops away quickly on cessation. Typical post-exercise findings include arterial bruits (distinctive local blood flow sounds on stethoscope examination) and absent or diminished pulses. Compression may occur at the origin of the medial head of gastrocnemius or plantaris, or as a result of the artery taking an aberrant course. Surgical removal of the compressive structure is usually indicated.

Nerve entrapment syndromes

‘Peripheral nerve entrapment’ describes the mechanical irritation by which a specific peripheral nerve becomes locally injured in a vulnerable anatomic site. These entrapments disturb the function of the nerve. Entrapment may occur at any site as a result of tissue damage, including fracture callus, haematomas or tumours. There are several anatomical sites where peripheral nerves run in relatively confined spaces and are therefore at increased risk of compression.

Sports physicians will need to consider other causes of neuropathies – degenerative, hereditary, vascular, inflammatory and metabolic diseases, all of which can damage nerves locally. Predisposing factors include repetitive activities involving the affected extremity, tenosynovitis, rheumatoid arthritis, acromegaly (growth hormone disorder), alcoholism, amyloidosis (a protein disorder), mucopolysaccharidosis (a metabolic disorder), gout, vitamin B6 deficiency, diabetes, trauma, and conditions altering fluid balance.

Nerve entrapments can exhibit variable clinical presentations similar to compartment syndrome, arterial entrapment and tendinopathy. Patients often describe the pain as sharp and shooting. Involved nerves may be sensory, motor or mixed.

The key to diagnosis of nerve entrapment is a detailed history followed by focused examination. Ideally patients should be examined post-exercise. The area of nerve innervation should be carefully evaluated and if it is possible to palpate the nerve, the clinician should percuss it along its course in order to identify the site of injury/entrapment. Spinal and central problems should be dealt with first, and diagnostic nerve blocks should be considered.

Lesions can occur at several points along a peripheral nerve trunk. In the ‘double crush syndrome’ (as postulated by Upton and McComas(2)), the presence of a lesion close to the body’s core does seem to increase the likelihood of peripheral nerve compression. Patients who may have double crush lesions should be identified ahead of any surgical procedure to release the entrapped peripheral nerve, as they are less likely to have an optimal outcome from surgery. Indeed, both entrapments may require treatment.

Sports-related lower limb nerve injury

i. Causes

Surgical:Peripheral nerves may become trapped from any incision. In orthopaedics, for instance, procedures such as bone graft harvest or ACL reconstruction may lead to nerve entrapment. Scars around the knee and ankle may entrap more superficial nerves.

Trauma: Direct trauma may cause nerve damage. Nerves may also be affected indirectly where the initial trauma is caused to closely related soft tissue, such as the psoas muscle and obturator nerve, the hamstrings and sciatic nerve or the medial collateral ligament and saphenous nerve.

Fascial pathology

a) Congenital

The concept of fascial (connective tissue) dysfunction was proposed by McCrory et al (2002)(3).The same fascial restriction that predisposes to muscle compartment syndromes may also envelop the neurovascular structures within the leg, resulting in either ischaemic or neural symptoms. This fascial dysfunction could explain why many athletes with chronic exercise-related leg pain appear to have a combination of different problems.

b) Traumatic

Excessive muscle use or strain can cause fascial tears. Nerves may be trapped in the resulting scar tissue or may bulge through the fascial defect itself.

ii. Investigations

Imaging techniques such as ultrasound or MRI scan can reveal structural or local inflammatory problems affecting nerves. Steroid/anaesthetic injections may be helpful in diagnosing or treating superficial sensory nerve entrapments but not those affecting the large motor nerves.

Nerve conduction studies allow the speed of nerve impulse propagation to be measured by placing electrodes on the patient’s skin. Electromyography requires fine needles to be placed directly into specific muscles, allowing their rates of contraction to be measured.

iii. Management

Most nerve entrapment syndromes will respond well to conservative treatment. Rest, ice or heat, nonsteroidal anti-inflammatory drugs (NSAIDS), massage and injections are frequently beneficial. Therapists should instruct their clients to avoid aggravating extrinsic factors such as tight shoes, straps or taping. Consider correction of performance where technique issues exist, a change of playing surface, and muscle strengthening or stretching work, as appropriate. Ultrasound, transcutaneous electrical nerve stimulation (TENS) and acupuncture may help, as may physiotherapy manipulation aimed at myofascial release.

Surgical intervention should be reserved for cases where the diagnosis is clear and the underlying cause has been identified. Clinical experience has shown that the best outcomes come from cases where there is a clear anatomical pain distribution, or where specific local weakness and/or nerve-related sensory symptoms exist. Non-specific leg pain or vague non-localising sensory symptoms should alert the therapist to alternative diagnoses. Nerve entrapment syndromes should not be diagnosed by exclusion.

Leg pain: neural pathologies

Below is a summary of sports-related common nerve entrapment syndromes. Anatomical details relate primarily to the common sites of entrapment.

Investigation and treatment options are similar for most of these syndromes, but special mention has been made where there is sufficient evidence to recommend specific management strategies for individual conditions.

Ilio-inguinal nerve (hockey player’s groin)

Anatomy

The first lumbar nerve divides into iliohypogastric and ilioinguinal branches which both run across the quadratus lumborum muscle to enter the abdominal muscles. The ilioinguinal nerve enters the inguinal canal, runs through it outside the spermatic cord and emerges through the superficial ring to supply the skin on the inner side of the scrotum/labia and adjoining thigh.

Pathology

Patients often complain of pain in this area when a hernia develops and presses on the nerve. The nerve can also be caught in post-hernia repair scarring. It is occasionally a primary entrapment. This condition and its treatment has been described primarily in hockey players (hockey player’s groin)(4). Presentation Pain in the inguinal region radiating into the genitals; sensory abnormalities in the distribution of the nerve; and tenderness on palpation 2 to 3cm medial to and below the ASIS suggest involvement of the ilioinguinal nerve(5).

Treatment

Physiotherapy can include techniques such as spinal mobilisation, psoas release, lower abdominal release and neural mobilisation. Surgical options can be release or division of the nerve.

Obturator neuropathy

Anatomy

Branches of the L2, L3 and L4 nerves fuse in the psoas muscle to form the obturator nerve. The nerve emerges from the medial psoas border just lateral to the sacrum. It then travels along the lateral wall of the lesser pelvis to enter the obturator foramen (nerve passage).

Just before entering the thigh, the nerve divides into an anterior and posterior branch. The anterior branch supplies motor innervation to adductor longus, brevis, gracilis and occasionally pectineus. It terminates in cutaneous, vascular and communicating branches. The cutaneous branch descends in the adductor canal to assist in the innervation of the skin and fascia of the lower two-thirds of the inner thigh.

The posterior branch pierces and supplies the external obturator muscle. It then runs between the adductor brevis and magnus muscles, splitting into a motor branch which supplies adductor magnus, and a sensory branch that descends to the knee joint, perforating the oblique popliteal ligament to supply the articular capsule, cruciate ligaments and synovial membrane.

Pathology

Obturator neuropathy was first described by Bradshaw et al. (1997)(6)in 32 patients, most of whom were Australian football players (26 patients). Bradshaw proposed that entrapment occurs when the anterior branch of the nerve is caught in the fascia over adductor brevis.

Presentation

There are many causes of chronic groin pain in athletes and the clinician should first try to exclude adductor muscle strain, stress fractures, osteitis pubis, psoas bursitis and inguinal hernia.

Obturator nerve entrapment is characterised by exercise-related medial thigh pain, centred on the adductor origin. Pain radiates down the inner thigh, with associated weakness. Pain or numbness in the inner knee area originating from the obturator nerve is known as the Howship-Romberg phenomenon.

Examination findings are painful passive abduction, painful/weak resisted adduction and tenderness at the pubic tubercle. After exercise there is weak resisted adduction and sometimes numbness in the lower/inner thigh.

As well as the use of nerve conduction studies and electromyography (EMG), MRI may demonstrate atrophy of the short and long adductor and gracilis muscles. Bone scan frequently shows a mild increase in uptake on the same side in the region of the pubic ramus at the origin of the short or long adductor muscle(6). Needle EMG shows denervation of the adductor muscles. Diagnostic nerve blocks can also be used.

Treatment

Treatment may consist of electrical stimulation of the adductor and hip flexor muscles, stretching and massage. These modalities, however, are typically successful only where the condition is recognised early. Surgical treatment involves releasing the anterior branch from its fascia and is effective.

Sciatic neuropathy/piriformis syndrome

Anatomy

The sciatic nerve is the largest nerve in the body and arises from the L4-S3 nerve roots in the pelvis. It passes through the greater sciatic notch into the buttock. Here the nerve runs vertically downward under the cover of the gluteus maximus, lying on the short muscles of the gluteal region midway between the greater trochanter and the ischial tuberosity. The sciatic nerve innervates the hamstring group of muscles.

Pathology

Sciatic trunk neuropathies may occur anywhere from the abdomen to the knee. A particular form of sciatic nerve entrapment has been reported in running athletes, where the nerve becomes entrapped at the level of the ischial tuberosity at the attachment of the biceps femoris muscle by either a fibrous aponeurotic band or a fibrous edge to that muscle. Surgical division of this fibrous structure cured the symptoms in the series of cases described by Puranen and Orava (1988)(7).

The ‘piriformis syndrome’ has been described as a specific form of sciatic entrapment in which the piriformis muscle compresses the nerve as it leaves the buttock just below the greater sciatic foramen. However its existence has been questioned. McCrory and Bell (1999)(8) suggest a better term would be ‘deep gluteal syndrome’, which encompasses several causative factors.

Presentation

Sciatic pain presents as tenderness in the buttock and more difficulty sitting than standing. Diagnosis is by provocative nerve tests, EMG and MRI.

Clinical signs for piriformis syndrome include positive straight leg raise, weakened abduction of the flexed thigh, and tenderness at the intersection of the muscle and nerve. The history of pain can be reminiscent of either compartment syndrome or arterial entrapment. Post exercise findings can be subtle but may include hamstring or distal weakness, especially on ankle eversion.

Treatment

If conservative treatments such as stretching and local injections are unsuccessful, surgery can be considered to divide adhesions beyond piriformis.

Common peroneal nerve entrapment

Anatomy

The common peroneal nerve (CPN) comes off the sciatic nerve in the mid-thigh and winds around the neck of fibula, where it can be palpated in the peroneal tunnel.

Pathology

Injury to the main trunk of the CPN in the region of the peroneal tunnel is frequently caused by some kind of external compression such as tight plaster casts, knee surgery, osteophytes, synovial cysts or ganglions, and sitting with legs crossed for prolonged periods.

The syndrome can also result from repetitive exercise involving inversion and pronation (eg: runners, cyclists), which stretches the CPN against the fibula and fibrous edge of the peroneal tunnel. This entrapment can present similarly to compartment syndrome and may co-exist.

Presentation

There may be tenderness around the head of fibula. It may be necessary to measure compartment pressure to differentiate the cause of pain. EMG/nerve conduction tests should be performed with exercise. Post-exercise findings include weakness and numbness in the nerve distribution.

Treatment

Watch out for predisposing activities, such as deep squatting in wicket-keepers or the use of tight knee braces. Surgical decompression generally works very well, though there is occasionally sensory loss behind the scar.

Lateral femoral cutaneous nerve (meralgia paraesthetica)

Anatomy

The lateral cutaneous nerve arises from L2 and L3. It runs across the iliacus muscle towards the top of the front of the hip bone, where it penetrates the inguinal ligament to emerge on to and supply the upper outer thigh.

Pathology

The nerve becomes trapped at the point where it passes through the inguinal ligament. Injury to the soft tissues in that area can lead to later entrapment.

Presentation

The patient will feel sharp lateral knee pain on acceleration, which often settles on running at full speed. There will be no knee joint signs, but there may be tenderness over the origin of the sartorius muscle. Pain may be reproduced with contraction of sartorius. There may be numbness over the distribution of the nerve, especially post-exercise.

Treatment

This entrapment may respond to local anaesthetic injection or to spinal, psoas, soft tissue release and neural stretches. Surgical release can be considered if these treatments fail.

Saphenous nerve

Anatomy

This is the terminal sensory branch of the femoral nerve and descends in the adductor canal and pierces the fascia over sartorius, travelling with the long saphenous vein. The two main branches are the infrapatellar, which supplies the skin under the knee, and the descending branch which supplies the skin over the medial malleolus (inner end of the tibia).

Pathology

The nerve crosses the inner aspect of the knee and can be involved in bursitis, MCL injuries and direct trauma. Damage can occur during orthopaedic surgery such as harvesting hamstring graft for ACL reconstruction or varicose vein surgery.

Presentation

There is medial knee pain with activity, especially after working the quadriceps. Pain may have a burning character and be present at night.

Treatment

Many patients improve with injections. In other cases destruction or removal of the infrapatellar branches can be considered.

Sural nerve

Anatomy

The tibial nerve is mainly motor, supplying the gastrocnemius, plantaris, popliteus and soleus muscles. All these branches arise within the popliteal fossa. The nerve also gives sensory branches to the knee joint and a large cutaneous branch that passes into the calf. Together with the communicating branch from the common peroneal nerve, this latter branch forms the sural nerve to run laterally with the short saphenous vein, supplying the skin on the outer edge of the foot.

Pathology

Although rarely a cause of exercise-related pain, compression of the sural nerve by mass lesions, scar tissue (eg post Achilles tendon repair), ganglia, surgical trauma and thrombophlebitis have all been reported. Extrinsic compression from tight ski boots and casts may similarly induce this problem.

Presentation

Symptoms can seem identical to Achilles tendinopathy. The nerve tends to be irritated higher up, often by a small muscle hernia. It can cause post-exercise numbness.

Treatment

Conservative treatment is preferable. Surgery works best when a specific point of entrapment is identified.

Tarsal tunnel syndrome (TTS)

Anatomy

Entrapments of the farther branches of the tibial nerve, most notably the posterior tibial nerve as it passes through the tarsal tunnel, are extremely common in sport. (The tarsal tunnel is a fibro-osseous tunnel formed by the flexor retinaculum, the medial wall of the calcaneus, the posterior aspect of the talus, distal tibia, and medial malleolus.)

Pathology

There are various theories as to why the nerve becomes compressed. These include tenosynovitis of the adjacent tendons, obesity, aberrant blood vessels and anomalous extra muscles – the latter is almost certainly the main cause in athletes.

Presentation

The syndrome can cause arch pain and heel pain. Examination findings include tenderness and a ropey feel to the nerve and a positive Tinel’s sign (pain on tapping the nerve). The medial calcaneal branch should also be palpated to see if it is irritated.

Treatment

In the first instance aim to correct biomechanical abnormalities using orthotics and footwear modifications. Local steroid or anti-inflammatory treatment may be useful. Where conservative measures fail surgical exploration may be appropriate.

Lateral plantar nerve

Anatomy

Cutaneous branches of the tibial nerve supply the skin over the heel. The nerve then divides into medial and lateral branches which supply their respective sides of the sole. The lateral plantar nerve accompanies the corresponding artery. Near the base of the fifth metatarsal it divides into superficial and deep branches which supply the remaining muscles of the sole.

Pathology

According to several recent anatomical and clinical studies, the entrapment of the lateral plantar nerve occurs between the deep fascia of the abductor hallucis muscle and the medial caudal margin of the quadratus plantae muscle.

Approximately 10% to 15% of athletes with persistent chronic heel pain have entrapment of the first branch of the lateral plantar nerve(9). Although runners and joggers account for the overwhelming majority of cases, this entrapment has been reported in athletes who participate in soccer, dance, tennis, and other track and field events.

Baxter and Thigpen (1984)(10) described a biomechanical basis for the entrapment in athletes. They proposed that the plantar nerves become stretched and trapped in the deep fascia of the abductor hallucis, combined with hypertrophy of the small foot muscles.

Treatment

The nerve can be surgically released.

Medial plantar nerve (jogger’s foot)

Anatomy

Similar to the lateral plantar nerve, the larger medial nerve accompanies the corresponding artery. The nerve also supplies abductor hallucis, flexor hallucis brevis, flexor digitorum brevis and the first lumbrical.

Pathology

Entrapment occurs at the crossing of the flexor digitorum longus and flexor hallucis longus tendons, on the inner side of the foot. Most patients are found to run with excessive heel valgus or with hyperpronation of the feet. Arch supports, especially those that are built up, may compress the nerve.

In 1978 Rask(11)termed entrapment of the medial plantar nerve jogger’s foot. Most char- acteristically there is tenderness on the plantar aspect of the medial arch in the region of the navicular tuberosity.

Treatment

As with the lateral plantar nerve, surgical release is effective.

Conclusion

Nerve entrapment syndromes are rare and difficult to diagnose definitively. The diagnosis is often ignored or neglected in favour of mechanical explanations. Treatment is often aimed at subtle benefits and every effort should be made to exclude alternative pathologies, confirm diagnosis and offer a full range of non-operative treatments. In the future hopefully we will have a better understanding of these syndromes and more accurate ways to image and test specific nerves.

References

1.Howard JL, Mohtadi NG, Wiley J (2000) ‘Evaluation of outcomes in patients following surgical treatments of chronic exertional compartment syndrome in the leg’ Clin J Sport Med10(3): 176-84

2.Upton AR, McComas AJ (1973) ‘The double crush in nerve entrapment syndromes’ Lancet 2(7825): 359-62

3. McCrory P, Bell S, Bradshaw C (2002) ‘Nerve entrapments of the lower leg, ankle and foot in sport’ Sports Med32(6): 371-91

4. Irshad K, Feldman LS, Lavoie C et al (2001) ‘Operative management of “hockey groin syndrome”: 12 years of experience in National Hockey League players’ Surgery130(4):759-64

5. Knockaert D, D’Heygere FG, Bobbaers H (1989) ‘Ilioinguinal nerve entrapment: a little known cause of iliac fossa pain’ Postgrad Med J65: 632-5

6. Bradshaw C, McCrory P, Bell S et al (1997) ‘Obturator nerve entrapment: a cause of groin pain in athletes’ Am J Sports Med25(3): 402-408

7. Puranen J, Orava S (1988) ‘The hamstring syndrome. A new diagnosis of gluteal sciatic pain’ Am J Sports Med 16: 517-21

8. McCrory P, Bell S (1999) ‘Nerve entrapment syndromes as a cause of pain in the hip, groin and buttock’ Sports Med27(4): 261-74

9. Schon LC, Baxter DE (1990) ‘Neuropathies of the foot and ankle in athletes’ Clin Sports Med9(2): 489-509

10. Baxter DE, Thigpen CM (1984) ‘Heel pain: operative results’ Foot Ankle5(1): 16-25

11. Rask MR (1978) ‘Medial plantar neuropraxia (jogger’s foot): Report of three cases’ Clin Orthop 134: 193

Nerve entrapment syndrome

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