Tibial nerve dysfunction
Tibial nerve dysfunction is a loss of movement or sensation in the lower leg, caused by damage to the tibial nerve.
Neuropathy - tibial nerve
Causes, incidence, and risk factors
Tibial nerve dysfunction is a form of peripheral neuropathy. It occurs when there is damage to the tibial nerve, one of the branches of the sciatic nerve of the leg. The tibial nerve supplies movement and sensation to the calf and foot muscles.
Dysfunction of a single nerve group, such as the tibial nerve, is called mononeuropathy. Mononeuropathy implies a local cause of the nerve damage, although occasionally systemic disorders may cause isolated nerve damage (such as occurs with mononeuritis multiplex).
The usual causes are direct trauma, prolonged pressure on the nerve, and compression of the nerve from nearby body structures. Entrapment involves pressure on the nerve where it passes through a narrow structure.
The damage may include destruction of the myelin sheath of the nerve (the insulation around the nerve) or destruction of part of the nerve cell (the axon). Damage to either part slows or prevents conduction of impulses through the nerve.
The tibial nerve is commonly injured by fractures or other injury to the back of the knee or the lower leg. It may be affected by systemic diseases causing polyneuropathy (damage to multiple nerves) such as diabetes. It may be damaged by pressure from lesions such as tumor, abscess, or bleeding into the knee.
In some cases, no cause can be identified.
Signs and tests
Neuromuscular examination of the legs shows tibial nerve dysfunction. There may be weakness or inability to push the foot downward (plantar flexion). Severe cases may cause wasting of the foot muscles and foot deformity.
Tests that reveal tibial nerve dysfunction may include:
- EMG (a recording of electrical activity in muscles)
- Nerve conduction tests (recording of electrical activity along the nerve)
- Nerve biopsy
Tests are done based on the suspected cause of the dysfunction suggested by the patient's history, symptoms, and pattern of symptom development. They may include various blood tests, x-rays, scans, or other tests.
Treatment is aimed at increasing mobility and independent self-care. In some cases, no treatment is required and recovery is spontaneous.
Surgical removal of lesions that press on the nerve may benefit some people.
Over-the-counter analgesics or prescription medications may be needed to control pain (neuralgia). Various other medications (phenytoin, carbamazepine, gabapentin or tricyclic antidepressants such as nortriptyline) may reduce the stabbing pains that some people experience. Whenever possible, medication use should be avoided or reduced to lessen the risk of side effects.
Physical therapy exercises may help some people maintain muscle strength. Orthopedic assistance may aid the ability to walk. This may include use of braces, splints, orthopedic shoes, or other appliances.
Vocational counseling, occupational therapy, job changes or retraining, or similar interventions may be recommended.
If the cause of the tibial nerve dysfunction can be identified and successfully treated, there is a possibility of full recovery. The extent of disability varies, with partial or complete loss of movement or sensation. Nerve pain may be quite uncomfortable and persist for a prolonged period of time.
- Partial or complete loss of foot movement
- Partial or complete loss of sensation in the foot
- Recurrent or unnoticed injury to the leg
- Deformity of the foot (mild to severe)
Calling your health care provider
Call for an appointment with your health care provider if symptoms of tibial nerve dysfunction are present. Early diagnosis and treatment increases the likelihood that symptoms can be controlled.
Prevention is variable depending on the cause of the nerve damage.
Feske S, Cochrane T. Degenerative and compressive structural disorders. In: Goetz, CG, ed. Textbook of Clinical Neurology. 3rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 29.
Reviewed By: David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine; and Daniel B. Hoch, PhD, MD, Assistant Professor of Neurology, Harvard Medical School, Department of Neurology, Massachusetts General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.