Sciatic Nerve

Original Editor - George Prudden

Top Contributors - George Prudden, Manisha Shrestha, Kim Jackson, Lucinda hampton, Candace Goh and Joao Costa

Description

The sciatic nerve is the largest nerve in the body, and consists of the medially placed tibial nerve and the laterally placed common peroneal nerve. It is formed from the ventral rami of the fourth lumbar to third sacral spinal nerves and is a continuation of the upper band of the sacral plexus.

The sciatic nerve is the largest nerve in the body, and consists of the medially placed tibial nerve and the laterally placed common peroneal nerve. It is formed from the ventral rami of the fourth lumbar to third sacral spinal nerves and is a continuation of the upper band of the sacral plexus.

It leaves the pelvis through the greater sciatic foramen, below the piriformis muscle, and descends between the greater trochanter of the femur and the ischial tuberosity. Initially deep to piriformis, it runs inferiorly and laterally posterior to the ischium, crossing over the nerve to quadratus femoris. Inferior to piriformis; it lies deep to gluteus maximus. It passes inferiorly crossing obturator internus, the gemelli and quadratus femoris. The posterior cutaneous nerve of thigh and the inferior gluteal artery lie on its medial side. Descending vertically, it enters the thigh at the lower border of gluteus maximus, where it lies on the posterior surface of adductor magnus. It gives off nerves to the hamstring muscles. The nerve is crossed obliquely on its superficial aspect by the long head of biceps femoris. The nerve ends at the upper aspect of the popliteal fossa by dividing into the tibial and common perineal nerves.

The nerve can be represented on the back of the thigh by a line drawn from just medial to the midpoint of the line from the ischial tuberosity to the apex of greater trochanter down to the apex of popliteal fossa.

It supplies articular branches to the hip joint, with muscular branches to biceps femoris, semitendinosus and semimembranosus and the ischial head of adductor magnus. The nerve to the short head of biceps is from the common peroneal division, with the other muscular branches emerging from the tibial division.

Branches

• Tibial nerve
• Common peroneal nerve

Clinical relevance

A great deal of variability exists in relationship of the sciatic nerve to the piriformis muscle and short external rotators. In approximately 85% of cases the sciatic nerve exits the pelvis deep to the muscle belly of the piriformis. It is usually superficial (posterior to the other external rotators). In 11% of individuals a portion of the piriformis muscle splits the common peroneal nerve and tibial nerve. These anatomic variations are important in the interpretation of intra-operative findings.

Piriformis Syndrome

Youngman described 'Piriformis Syndrome' in 1928 as an evolving compression of the sciatic nerve by the piriformis muscle. This is associated with acute trauma to the buttock and occurs when the sciatic nerve exits posterior to the piriformis. The patient finds sitting difficult and participation in activities where hip flexion or internal rotation is required, almost impossible. The pain is in the sciatic nerve distribution.

Physical examination reveals tenderness directly over the piriformis tendinous or in the gluteal area, and the pain can be listed by forced internal rotation of the extended thigh – this is sometimes called 'Pace's sign'. There is sometimes weak abduction against resistance or external rotation against resistance, and the pain may also be reproduced by rectal or vaginal examination.

Treatment involves rest and oral anti-inflammatory drugs. The diagnosis can also be confirmed by the injection of local anesthetic under fluoroscopy into the area of injury. Steroid injection may occasionally be necessary. In refractory cases, surgical exploration of the piriformis and/or division of the piriformis muscle and/or mobilization of the sciatic nerve may be necessary.

The piriformis syndrome is thought to be due to irritation of the sciatic nerve as it passes over the piriformis tendon. This causes buttock pain and sciatica. The pain can be reproduced by applying pressure to the piriformis fossa on the posterior aspect of the greater trochanter and by stressing the piriformis muscle. Injections can once again be diagnostic and therapeutic. Some authors have reported good results by sectioning the piriformis to relieve the pain.

Hamstring Syndrome

This pathology commonly affects athletes who present with localised and radiating pain near the ischial tuberosity. The pathophysiology is thought to be that of an insertional tendopathy at the ischium but there may also be involvement of sciatic nerve compression. The pain in hamstring syndrome radiates down the posterior thigh or popliteal region and is exacerbated when the hamstrings are on tension. This is often seen in sprinters or hurdlers. On examination there is exquisite tenderness over the ischial tuberosity and percussion in that region may reproduce the sciatic distribution of pain. Treatment involves rest, anti-inflammatory agents and steroid injections.

Hip Dislocation

In view of the high intrinsic stability of the hip, hip dislocations are almost always due to high-energy trauma and require careful assessment. Such injuries typically occur in motor vehicle accidents, falls from great heights and industrial injuries. Regardless of the type of activity involved, the pathological force is transmitted to the hip joint and arises from one of three common surfaces:

• The anterior surface of the flexed knee striking an object.
• The sole of the foot striking an object with the ipsi-lateral knee extended.
• A blow to the greater trochanter.

In more rare circumstances, the dislocation force may be applied to the posterior pelvis with the ipsi-lateral foot only acting as a counter-force. The injury sustained depends upon the amount and direction of force and the quality of bone in the proximal femur and acetabulum.

The classic posterior dislocation of the hip is a dashboard injury where, after rapid deceleration, the body pivots forward and the knee strikes the dashboard with the hip and knee both flexed at 90 degrees. This tends to force the femoral head up posteriorly. If the hip is less flexed at the time of impact, the femoral head strikes the posterior or postero-superior aspect of the acetabulum leading to a fracture dislocation. The amount of hip rotation at the time of impact will influence both the direction and type of dislocation or fracture dislocation. During hip dislocation the femoral head fractures impactions or articular scratches are commonly seen. These can range from tiny cartilaginous avulsion fragments to major osteocartilaginous injuries of the femoral head. Such fragments can become incarcerated between the femoral head and the acetabular articular surface following reduction of dislocation and lead to incongruity and long term degenerative changes.

Femoral neck fractures may be associated with femoral head dislocations both because of the high energy at the time of trauma and also because of the forces required during reduction. The severe forces required in order to dislocate the femoral head are such that the threshold deformity for chondrocyte death may be exceeded. This may be one potential explanation for the high incidence of traumatic arthritis following hip dislocation. The fact that osteocartilaginous fragments are also displaced and/or lost is another significant contributing factor. Any significant loss of normal articular congruence or articular contact secondary to femoral head depression or defects seems to predispose to rapid degenerative change.

Avascular necrosis of the femoral head secondary to vascular embarrassment at the time of hip dislocation is also a common consequence. The incidence in literature varies from 1% to 70%. This may be particularly related to incidences where the hip is left dislocated for a long period. The latter suggests that there may be a number of mechanisms for osteonecrosis. Firstly, there may be an immediate complete disruption of the blood supply and to the femoral head at the time of violent dislocation. Later there may be a slower process where prolonged abnormal stretching of the arterial supply leads to spasm or thrombosis. Finally, there could be a venous thrombus tension and the vascular drainage leads to venous occlusion, back pressure and ultimate arterial obstruction. The latter two mechanisms can be influenced by early and rapid reduction of the dislocated hip.

The natural history of post-traumatic osteonecrosis of the femoral head may be different from that of idiopathic osteonecrosis in that isolated segments may go on to sclerosis and collapse without the rest of the femoral head being affected. This may affect the type of salvage procedure that is performed.

Hip dislocations are secondary to high-energy trauma and therefore are often associated with multi-system injuries. It is particularly important to examine for occult knee ligament injuries and for sciatic nerve injuries. The common peroneal division of the sciatic nerve is most commonly involved. Great care is required when there is a concomitant femoral fracture and this may mask the otherwise obvious hip dislocation.

Hip dislocations are typically sub-divided into anterior or posterior. The so called central dislocation of the hip is essentially an acetabular fracture. Thompson and Epstein have classified posterior hip dislocations. A 'Type 1' dislocation is a pure dislocation with an insignificant posterior wall fragment. A 'Type 2' dislocation is associated with a single large posterior wall fragment. A 'Type 3' dislocation is a comminuted distal wall fracture, and a 'Type 4' fracture dislocation is an acetabular floor fracture. A 'Type 5' dislocation is complicated by femoral head fracture. Pipkin has classified posterior hip dislocations associated with femoral head fractures based on the location of the femoral head fracture. With a 'Type 1' injury the femoral fracture is inferior to the fovea centralis. In a 'Type 2' injury the fracture line extends superior to the fovea centralis and typically includes the fovea. In a 'Type 3' injury the femoral head fracture is associated with the femoral head fracture, and in a 'Type 4' injury the femoral head fracture is associated with an acetabular fracture.

Such classification systems help to guide treatment particularly now that CT scanning and MRI are widely available.

In Type 1 hip dislocation the hip can typically be reduced with ease. This is best done with sedation and/or anesthesia with the availability of image intensification. No great force or leverage should be applied lest the femoral neck should be fractured. Post-reduction films would typically demonstrate a concentric reduction with no widening of the joint and no incarcerated fragments between the articular surfaces. CT scan can confirm this. A small bone fragment within the acetabular fossa secondary to a ligamentum teres avulsion is thought to be a benign finding that does not require surgical intervention. Management of posterior hip dislocations are based on a congruent reduction, the restoration of normal articular surfaces and the restoration of hip stability. This can be achieved in a number of ways by addressing inroads to the acetabulum, posterior wall, the femoral head and the soft tissues respectively.

Anterior hip dislocations are classified on the basis of their location. Their prognosis is far less favorable than previously thought. They can also be classified according to their stability such that Type 1 injuries have no significant associated fractures and no clinical instability following concentric reduction. Type 2 injuries are irreducible dislocations without significant femoral head or acetabular fracture. Irreducible in this setting implies that a reduction has been attempted under general anesthesia with muscle paralysis. Type 3 injuries are unstable hips following reduction due to incarcerated fragments of cartilage or bone. In Type 4 injuries there is an associated acetabular fracture requiring reconstruction to restore hip stability or joint congruity. In Type 5 injuries there is associated femoral neck injury.

Computerized tomography with multiple bony cuts through the hips and sacro-iliac joints is often very helpful. 1mm slices allow a very accurate three-dimensional CT reconstruction. Magnetic resonance imaging is very useful to evaluate the soft tissues and to later verify the vascularity of the femoral head.

Management of acetabular dislocations involves a reduction as early as possible. Regardless of the direction on the dislocation, reduction can be attempted with in line traction with the patient lying supine. This is preferably performed under general anesthesia. The most common method is to apply traction in the line of the deformity. Someone should apply counter-traction by stabilizing the patient's pelvis. If a hip cannot be reduced by closed manipulation under general anesthesia, then immediate open reduction must be performed if the patient's general condition or other injuries allow this. The approach used will be determined by associated acetabular and femoral head injuries.

The typical problems associated with hip dislocations are missed and delayed diagnosis, particularly in a multiply injured patient, osteonecrosis, traumatic arthritis, recurrent dislocation, sciatic nerve injury. Post-surgical complications include infection, sciatic nerve injury, both early and late heterotopic ossification and thrombo-embolism.

The femoral head is supplied by three terminal arterial sources: the artery of the ligamentum teres, a terminal branch of the lateral femoral circumflex artery and the terminal branch of the medial circumflex artery, the lateral epiphyseal artery. The latter is the critical blood supply to the majority of the weight bearing superior portion of the femoral head. This artery is particularly at risk during posterior fracture dislocation. The adult femoral head ranges in diameter from 40mm to 60mm and is not a perfect sphere. Its subtle ace veracity is reflected on the acetabular side. Accurate reduction of femoral head fragments is necessary in order to maximize contact area between the femoral head and the acetabulum and to minimize stresses across the articular cartilage. The management of femoral head fractures involves adequate imaging with plain X-rays and CT scans followed by open reduction and internal fixation. The specific procedure undertaken will depend on any associated hip instability and/or acetabular injuries.

Kocher-Langenbeck Approach (Posterior Approach)

Standard posterior approach to the hip is the 'Kocher-Langenbeck' approach. This is typically performed in a lateral decubitous position without use of a traction table. After splitting the gluteus maximus muscle, the sciatic nerve is identified and examined for contusion, hemorrhage or partial or complete laceration. The gluteus maximus must not be split too proximally as this can lead to denervation secondary to injury of the inferior gluteal nerve. After identifying the sciatic nerve, the tendinous insertions of the piriformis muscle and the obturator internus are identified and tagged with heavy absorbable sutures. If torn, they are detached and retracted. Care must be taken not to injure the acetabulum labrum when performing capsulotomies. Quite frequently, however, capsulotomies have already been created by the injury. The joint can then be assessed, any fracture fragments removed or stabilized and the entire area thoroughly washed out.

Anterior Approach

The anterior approach to the hip for injuries can be performed through the 'Smith Peterson' or 'Watson Jones' approaches. These can be performed with the patient in the semi-lateral or lateral dicubitous position. The latter has particular advantages if a simultaneous or posterior approach is also to be considered.