Answer:
Femoral nerve: L2-L4, supplies the quadriceps and anteromedial thigh, continues as saphenous nerve; saphenous nerve supplies the skin over medial side and front of the knee, medial leg and skin on the medial and dorsal side of the foot.
Sciatic nerve: L4-5, S1-3, branches into tibial and common peroneal nerves.
Tibial nerve: (from anterior branches of lumbosacral plexus) supplies muscles of posterior thigh and leg (superficial and deep compartments); continues as the medial and lateral plantar nerves (analogous to the median and ulnar nerves of the hand, respectively). Palsy results in a cavus deformity due to plantar fascia contracture and lengthening of the Achilles tendon rotating the calcaneus into dorsiflexion.
Common peroneal nerve: supplies short head of biceps femoris in thigh; divides into superificial and deep nerves; deep peroneal nerve supplies the muscles of the anterior compartment and a sensory component to the 1st web space; superficial peroneal nerve supplies the muscle of the lateral compartment of the leg and sensation to the lateral distal leg and dorsum of the foot. Palsy results in foot drop and paresthesias.
Although improved microvascular techniques have allowed for nerve repair and nerve grafting, the results of nerve repair and grafting in the lower extremity have been poor. These poor results are in part due to the long distance from the spinal cord and the motor end plates, the complex distribution of nerve fascicles, and the long distance required for the nerve to grow to the motor end plate, resulting in end-organ atrophy. Recent experience with nerve grafting has shown some promising results. Trumble found an average return of strength of 11% and protective sensation in all of 9 patients treated with nerve grafts for repair of the peroneal and sciatic nerves. However, most of these patients were in the pediatric age group.
Disruption of the peroneal nerve results in foot drop and loss of sensation of the dorsum of the foot. Although not crippling, lifelong foot splinting or tendon transfers are required to offset the foot drop. The loss of sensation of the dorsum of the foot does not cause much morbidity. The loss of the posterior tibial nerve is more devastating. It results in the loss in plantar flexion of the foot, which facilitates the step-off in ambulation. The most devastating loss is the loss of sensation of the plantar aspect of the foot. It results in the loss of some position sense and in chronic injury and wounding of the plantar aspect of the foot. Atrophy and vasomotor changes complicate the injury and may often result in amputation. Though not an absolute indication for amputation, as it is not much different from the foot of the patient with diabetic neuropathy, it may be a relative contraindication.
Nerve injuries to the lower extremity should be repaired at the time of injury if primary repair can be achieved. If nerve grafts are necessary to bridge nerve gaps, they are perhaps best delayed until a healthy soft tissue bed is established. The prognosis of nerve repair is guarded at best, and most patients require tendon transfers or lifetime splinting.