Tibial nerve injuries …

Mazen M Dimachkie MD

General Neurology

Updated 07.06.2024
Released 07.14.1999
Expires For CME 07.06.2027

Tibial nerve injuries

Author: Mazen M Dimachkie MD

See Contributor Disclosures

Editor: Randolph W Evans MD

Tibial nerve injuries

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Clinical manifestations

Presentation and course

Tibial nerve injuries are best considered based on anatomic alignment. The divisions are arbitrary but include the proximal tibial nerve, the distal tibial nerve or plantar nerves (including the individual plantar nerves at or distal to the tarsal tunnel), the interdigital nerves, and the sural nerve.

Proximal tibial nerve. Due to its anatomic location, damage solely to this nerve is rare. It has been associated with bakers cysts (06), trauma to either the knee or ankle, nerve sheath tumors (19), soleus muscle tendinous arch entrapment (28), and a host of rare and unusual causes, including posterior tibial nerve impingement from a tibial spine fixation screw (22). Tibial nerve injuries have been reported following subfascial endoscopic perforating vein surgery (08).

Popliteal artery injury after a fracture around the knee area and the subsequent hematoma-complicating repair of such artery can cause compression neuropathy of this nerve (and the common peroneal nerve) in a chronic and progressive manner (24).

Due to the proximal nature of these lesions, patients present with weakness of foot plantar flexors and foot invertors, long toe flexors, and intrinsic foot muscle. Sensory loss usually involves the sole of the foot. It is important during the physical examination to palpate the popliteal fossa, looking for evidence of a mass such as a Baker cyst or neoplasm.

Distal tibial and plantar nerves. The tibial nerve and its terminal branches, the medial and lateral plantar, and medial calcaneal can be compressed within the tarsal tunnel (the roof of which is formed by the flexor retinaculum) at the ankle.

Distal tibial and plantar nerves

The tibial nerve and its terminal branches, the medial and lateral plantar and medial calcaneal, can be compressed within the tarsal tunnel, the roof of which is formed by the flexor retinaculum at the ankle. (Contributed by Dr. A...

The most common pathology relates to external compression from shoes that are too tight or to plaster casts. Associations include posttraumatic fibrosis, tendon sheath cysts, rheumatoid arthritis, and hypothyroidism. The plantar nerves may be damaged within the tarsal tunnel or more distally as they course through the arch and sole of the foot. The medial plantar nerve is injured more commonly than the lateral.

Clinical manifestations include foot and ankle pain along with paresthesias in various areas on the sole of the foot, depending on the particular terminal nerve involved. If there is sensory loss on the heel, the medial calcaneal sensory branch is usually involved, localizing the lesion within or proximal to the tarsal tunnel.

Digital neuropathies (Morton neuromas). The interdigital nerves can become compressed between the adjacent metatarsal heads or stretched where they cross the deep metatarsal ligament (13). Although debated, the nerve in the third metatarsal interspace is most frequently involved. Joplin neuroma refers to a digital neuroma on the medial side of the great toe being compressed by ill-fitting shoes or scarring after bunion surgery (11).

Sural neuropathy. The sural nerve can be injured from a Baker cyst in the popliteal fossa or, more distally, by vein stripping or compression. The most common cause of an isolated sural neuropathy is nerve grafting or biopsy. After biopsy, the nerve may occasionally become hyperpathic, with unpleasant or painful paresthesias experienced over the lateral ankle and foot. The sural nerve can also be injured at the ankle by tendon sheaths and scar tissue. Sural nerve entrapment localized to its course as it passes through the superficial sural aponeurosis is described in athletes. Such entrapment results in chronic calf pain, exacerbated by physical exertion. Electrodiagnostic testing may be helpful in making the diagnosis. The results of surgical decompression are encouraging (07). In 36 cases, isolated sural mononeuropathy was mostly posttraumatic (18/36), but in some cases, it was related to benign compression, neurofibromatosis, or cellulitis (32). Interestingly, seven cases were associated with an autoimmune disorder such as Sjogren syndrome, rheumatoid arthritis, psoriasis, cryoglobulinemia, nonsystemic vasculitic neuropathy, or histiocytic vasculitis, and two of these cases were treated with steroids and improved. Three patients had sural nerve biopsies, and these demonstrated focal demyelination, vasculitis, or mild axonal loss.

Prognosis and complications

Causalgia can result from tibial nerve injury as well as sural nerve biopsy (18). Tibial nerve injury affecting foot intrinsic muscles can also result in clawing of the toes. Prognosis depends on the degree of nerve injury.

Clinical vignette

Compared to lesions of most other major limb nerves, tibial neuropathies are rare. The proximal tibial nerve lies deeply in the popliteal fossa and the calf and is, thus, protected from external compression in these areas. We report a case of proximal tibial mononeuropathy that occurred during a lower extremity vascular intervention, presumably caused by embolic occlusion of the vasa nervorum.

Case report. A 55-year-old man with a history of insulin-dependent diabetes mellitus, hypercholesterolemia, atherosclerotic heart disease, and tobacco use was undergoing percutaneous transluminal angioplasty of his right superficial femoral artery and percutaneous transluminal angioplasty or stent placement in his left common iliac artery for hip and calf vascular claudication. From a prior angiogram, the patient was known to have aortic atherosclerosis, with a moderate focal stenosis at the origin of the right internal iliac artery filling distally via collaterals from the left internal iliac branches, superficial and deep iliac circumflex arteries, and external pudendal artery. Other findings on the right included occlusion of the superficial femoral artery over a 5 cm segment in Hunter canal with collaterals reconstituting it in the distal canal, occlusion of the anterior tibial artery at the ankle, but a patent posterior tibial artery at the foot. On examination, the patient had normal femoral pulses, with no pulse in the popliteal and dorsal pedal arteries and reduced pulses in the posterior tibial arteries. Pulse volume recordings showed a right ankle-brachial index of 0.67 and left ankle-brachial index of 0.83.

The percutaneous transluminal angioplasty procedure involved a left circumferential femoral artery approach. The patient was awake during it, watching the monitor. When the catheter was advanced within his right leg, he suddenly experienced pain in the right foot, most severe over the sole. Postangioplasty, his pulse volume recordings had improved to 1.0 bilaterally. A duplex ultrasound of the lower extremities revealed a remote thrombus at the left saphenofemoral junction. He was discharged. During follow-up visits, he complained of severe shooting pain and electric sensation in his right foot along with hypersensitivity. He was given a trial of capsaicin cream and amitriptyline without relief.

A neurologic consultation was performed one month after the interventional procedure. At that time, examination disclosed obvious atrophy of the right calf muscles.

Foot diagram

Diagram of the tibial nerve and its divisions. (Contributed by Dr. Asa Wilbourn.)

Motor strength testing was 5/5 (5 being normal based on the Medical Research Council scale) bilaterally for the hip flexors and extensors and knee flexors and extensors. The right foot dorsiflexors were 4.5, plantar flexors 4, invertors 4, and evertors 5; the right extensor hallucis longus was 3.5. On the left side, all motor strength testing scores were 5. The right ankle deep tendon reflex was unelicitable; the remaining lower extremity deep tendon reflexes were normal. Sensory testing showed hyperpathia along the lateral border of the right foot. There was decreased sensation to pinprick on the right foot in the tibial nerve distribution and decreased vibration on the great toes bilaterally with normal proprioception. The patient walked with a limp on the right and could neither hop nor toe-walk on the right foot.

The electrodiagnostic examination revealed, on nerve conduction studies, loss of the right medial and lateral plantar nerve action potentials, with normal sural and superficial peroneal nerve conduction study responses. The right posterior tibial motor nerve conduction study responses were unelicitable in abductor digiti quinti pedis recording and low in amplitude in abductor hallucis recording. The right peroneal motor nerve conduction study responses were normal, recording extensor digitorum brevis. All the nerve conduction studies reported above were also performed on the asymptomatic left lower extremity and were normal. The right H response was absent, and the direct motor response recorded from the gastrocnemius and soleus muscle group during the H-wave test was significantly lower in amplitude on the right when compared to the left. Needle electrode examination revealed fibrillation potentials and substantial loss of motor unit potentials in the right soleus, medial and lateral gastrocnemius, flexor digitorum longus, tibialis posterior, abductor hallucis, and abductor digiti quinti pedis muscles. Needle electrode examination was normal on the right gluteus maximus, vastus lateralis, biceps femoris (short and long head), tibialis anterior, extensor hallucis longus, peroneus longus, extensor digitorum brevis, and high sacral paraspinal muscles. In addition, the needle electrode examination of the left lower extremity showed no abnormalities.

The electrodiagnostic findings were suggestive of a right tibial mononeuropathy, axon loss in type, located in the popliteal region; the lesion appeared to be situated proximal to the motor branch to the gastrocnemius muscles yet distal to the origin of the tibial component of the sural nerve.

Discussion. In contrast to common peroneal neuropathies, tibial mononeuropathies of all types are rare (if tarsal tunnel is not included). The presumed etiology of the tibial neuropathy in our case was infarction of the tibial nerve in the proximal popliteal fossa. Most likely, the infarction was secondary to an atherosclerotic embolus within an already compromised superficial femoral circulation. It is important for consulting neurologists and vascular surgeons to be aware of this complication.

Plantar aspect of the left foot

Diagram showing the various neuropathies of the foot: medial plantar, lateral plantar, saphenous, calcaneal, and sural. (Contributed by Dr. Asa Wilbourn.)

Biological basis

Etiology and pathogenesis

The tibial nerve arises from the larger, medial portion of the sciatic nerve; it usually grossly separates from the sciatic nerve at the level of the middle to the distal third of the thigh. With the common peroneal nerve, the other derivative of the sciatic nerve, it lies deep in the hamstrings. In the proximal thigh, it supplies all the hamstrings (except the biceps femoris short head). In the popliteal area, it usually lies posterior to the popliteal artery and vein. Sensory branches typically leave the tibial nerve in the proximal calf before major motor branches arise. The nerve tends to run beneath the gastrocnemius-soleus muscle, supplying branches to the plantaris, popliteus, and tibialis posterior as well as the gastrocnemius-soleus. A deep or posterior tibial branch (or nerve) arises from it and accompanies the tibial artery and vein to run through the leg, medial and posterior to both the tibia and to the intermuscular septum separating anterior from posterior compartments. The posterior tibial nerve carries fibers destined for the foot, but it gives off motor branches in the more proximal leg to supply the flexor digitorum and flexor hallucis longus. As the posterior tibial nerve approaches the ankle, it courses inferior to the medial malleolus and branches into the medial and lateral plantar nerves as it passes beneath the medial collateral ligament. The medial plantar nerve supplies the intrinsic foot muscles on the medial aspect of the foot and sensation to the medial aspect of the foot. The lateral plantar nerve runs deep in the instep and supplies the foot intrinsic muscles on the lateral aspect of the foot as well as sensation to the lateral portion of the sole of the foot. A medial calcaneal branch can often be found arising either proximal to these nerves or arising from the medial one. It provides sensation to the heel.

Unilateral nerve injury can cause profound, long-lasting, nerve branch-specific loss of distal innervation both contralaterally and ipsilaterally (23). This study was conducted in rats, but it does lend credence to the fact that homologous nerves may be affected when there is unilateral injury.

Diagnostic workup

As with all aspects of neurology, a good history and physical examination are important. It is important during the examination to evaluate the gluteal muscles and hamstrings. The popliteal fossa should be palpated for masses and the knee and foot for Tinel sign. In tarsal tunnel syndrome, a Tinel sign producing paresthesias on the bottom of the foot is usually present inferior to the medial malleolus and sometimes proximally or distally to the instep.

As an example of sensory innervation, the posterior tibial nerve supplies sensation to the foot, giving rise to calcaneal (heel) and medial and lateral plantar nerves. The sural nerve supplies the lateral side of the foot, and the saphenous nerve a patch below the medial malleolus. Complete tibial nerve injury results in sensory loss on the sole and heel of the foot. In terms of electrodiagnostic evaluation, most lesions are axon loss in type; consequently, the amplitude of the tibial motor conduction studies recording both abductor hallucis and abductor digiti quinti pedis is often affected. Also, with lesions proximal to the popliteal fossa the amplitude of the direct muscle response (M component) of the H-reflex is often low, and the H-wave unattainable. Lesions proximal to the popliteal fossa will also affect the amplitude of the sural response, but usually this is normal because the lesions are in the popliteal fossa or more distal. With S1 radiculopathies the sural nerve conduction study's response is normal, whereas it is usually low in amplitude or unelicitable with sacral plexopathies or sciatic neuropathies. Sensory nerve responses can also be obtained for medial calcaneal nerve; conduction latencies, amplitudes, and sensory nerve conduction velocities are significantly less in patients with plantar fasciitis (03). The needle electrical examination can be helpful for localization by revealing which muscles are affected and which are not. The needle electrode examination assessment must also include limb muscles innervated by the common peroneal as well as the tibial nerve (03).

Tumors may require MRI using gadolinium enhancement. Soft tissue tumors in the popliteal space may be seen with plain film radiographs, ultrasonography, or computerized axial tomography scanning. Arthrograms and arteriography can be useful for Baker cysts and popliteal aneurysms.

In a preliminary report, high-resolution MR neurography (MRN) was promising and yielded accurate morphologic information about the location and extent of nerve injury after failed tarsal tunnel release (05). MRN studies were reviewed in nine patients (10 legs) referred for failed tarsal tunnel release. Nine studies (90%) had findings of nerve re-entrapment related to focal fibrosis, with MRN sensitivity of 77% for posterior tibial nerve, 100% for medial plantar nerve, and 100% for lateral plantar nerve injury. The sensitivity of MRN was 67% for neuroma detection. Normal values for the ratio of fractional anisotropy to apparent diffusion coefficient on diffusion tensor imaging (DTI) have been established in 25 normal controls, and more is to be learned about the usefulness of this novel method in diseased sural nerves (14). In another study using DTI tractography to image 26 cases of soft tissue peripheral nerve tumors, DTI was found to be possibly helpful in assessing peripheral nerve infiltration by malignant tumors, but more studies are needed (12).

Management

Management depends on the problem. In cases of compression, removal of the compressive force is the first step. Baker cysts can be removed surgically as can many nerve sheath tumors. Tarsal tunnel syndrome treatment, at least initially, should be conservative. When conservative measures fail, surgical release may be considered. Krishnan and colleagues described a novel technique of endoscopic in situ decompression in eight patients with moderate to severe compression of the tibial nerve at the tarsal tunnel who had failed conservative management (15). All patients had an outcome rated good to excellent, with neurodiagnostic normalization in six of eight patients. A more extensive surgery may be needed to effectively decompress the tibial nerve and its branches in tarsal tunnel syndrome (25). In addition to roof incision, this involves decompression of the medial plantar and lateral plantar nerves and the excision of the inter-tunnel septum. There is an increasing interest in acupotomy for treating tarsal tunnel syndrome. This modification of acupuncture uses a modified needle that is bladed and has a flat head and cylindrical body. Acupotomy is widely used as part of traditional Chinese medicine. A systematic review of acupotomy for the treatment of tarsal tunnel syndrome in ongoing (29). In a systematic review of the management of tarsal tunnel syndrome, the authors suggest that surgical treatment should be reserved for a very select group of cases refractory to medical or minimally invasive options (30).

The unique combination of plantar fasciitis, posterior tibial tendon dysfunction, and tarsal tunnel syndrome is referred to as “heel pain triad.” Labib and colleagues found that those who manifested this triad improved after surgery 85% of the time (16). Surgical success is debatable, and many patients have multiple surgeries with worsening symptoms. Though similar improvement by objective measurements was noted in a series of 68 surgeries, 51% of patients reported persistent symptoms following tarsal tunnel release (09). The superficial peroneal nerve is a valuable nerve donor site, particularly when multiple long grafts are needed for large motor and sensory defects (01). Physical therapy and orthotic devices should also be investigated when deemed appropriate.

Initial management of Morton neuromas is also conservative, consisting of shoe modifications and steroid injections. Though the difference in improvement between steroid injections with shoe modification and shoe modification alone was not statistically significant at 12-month follow-up, Saygi and colleagues reported a trend toward better outcome and a significant difference in patient satisfaction in those receiving steroid injections (27). Haddad-Zebouni and colleagues reported near complete regression of Morton neuroma on MRI following steroid injection (10). Fifty-eight subjects diagnosed with Morton neuroma and foot pain of at least four were locally injected with capsaicin 0.1 mg or blinded placebo (02). At weeks 1 and 4, there was statistically significant pain reduction in the capsaicin group as compared to placebo, and at weeks 2 and 3, a trend towards capsaicin benefit was observed. The capsaicin-treated group had improvements in functional interference scores and reductions in oral analgesic use. This study provides preliminary evidence that local capsaicin injection may be a short-term therapy effective in reducing pain in patients with Morton neuroma. A study showed no difference in outcomes between patients injected with a corticosteroid plus a local anesthetic as compared to a local anesthetic alone (17). In a long-term study of the treatment of Morton neuroma, ultrasound-guided injections yielded better outcome than blind injections for up to three years (26). In a systematic review of infiltrative treatment for Morton neuroma, six randomized controlled trials and six longitudinal observational studies were identified (21). Corticosteroids were highly effective. Capsaicin reduced pain in half. Alcohol or hyaluronic acid injections needed further data from controlled studies. In contradistinction, a 2024 Cochrane review of Morton neuroma concluded that corticosteroid and local anesthetic injection resulted in little to no pain relief (20). However, ultrasound guidance while injecting this combination reduces pain and improves function.

Media

References

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03: Chang CW, Wang YC, Hou WH, Lee XX, Chang KF. Medial calcaneal neuropathy is associated with plantar fasciitis. Clin Neurophysiol 2007;118(1):119-23. PMID 17095287
04: Cherian RP, Li Y. Clinical and electrodiagnostic features of nontraumatic sciatic neuropathy. Muscle Nerve 2019;59(3):309-14. PMID 30414322
05: Chhabra A, Subhawong TK, Williams EH, et al. High-resolution MR neurography: evaluation before repeat tarsal tunnel surgery. AJR Am J Roentgenol 2011;197(1):175-83. PMID 21701028
06: DiRisio D, Lazaro R, Popp AJ. Nerve entrapment and calf atrophy caused by a Baker's cyst: case report. Neurosurgery 1994;35:333-4. PMID 7969847
07: Fabre T, Montero C, Gaujard E, Gervais-Dellion F, Durandeau A. Chronic calf pain in athletes due to sural nerve entrapment: a report of 18 cases. Am J Sports Med 2000;28(5):679-82. PMID 11032224
08: Geselschap JH, van Gent WB, Wittens CH. Complications in subfascial endoscopic perforating vein surgery: a report of two cases. J Vasc Surg 2001;33(5):1108-10. PMID 11331858
09: Gondring WH, Shields B, Wenger S. An outcomes analysis of surgical treatment of tarsal tunnel syndrome. Foot Ankle Int 2003;24(7):545-50. PMID 12921360
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11: Joplin RJ. The proper digital nerve vitallium stem arthroplasty, and some thoughts about foot surgery in general. Clin Orthop 1971;76:199-212. PMID 5578142
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13: Kite JH. Morton's toe neuroma. South Med J 1966;59:20-5. PMID 5902751
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15: Krishnan KG, Pinzer T, Schackert G. A novel endoscopic technique in treating single nerve entrapment syndromes with special attention to ulnar nerve transposition and tarsal tunnel release: clinical application. Neurosurgery 2006;59(1 Suppl 1):ONS89-100. PMID 16888558
16: Labib SA, Gould JS, Rodriguez FA, Lyman S. Heel pain triad (HPT): the combination of plantar fasciitis, posterior tibial tendon dysfunction, and tarsal tunnel syndrome. Foot Ankle Int 2002;23(3):212-20. PMID 11934063
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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Mazen M Dimachkie MD

Dr. Dimachkie, Director of the Neuromuscular Disease Division and Executive Vice Chairman for Research Programs, Department of Neurology, The University of Kansas Medical Center received consultant honorariums from Abata/Third Rock, Abcuro, Amicus, ArgenX, Astellas, Cabaletta Bio, Catalyst, CNSA, Covance/LabCorp, CSL Behring, Dianthus, EMD Serono/Merck, Horizon, Ig Society Inc, Ipsen, Janssen, Octapharma, Priovant, Ra Pharma/UCB Biopharma, Sanofi Genzyme, Shire/Takeda, Treat NMD/TACT, and Valenza Bio. Dr. Dimachikie also received research grants from Alexion/Astra Zaneca, Amicus, Astellas, Catalyst, CSL Behring, EMD Serono/Merck, Genentech, Grifols, GSK, Horizon, Janssen, Mitsubishi Tanabe Pharma, MT Pharma, Novartis, Octapharma, Priovant, Ra Pharma/UCB Biopharma, Sanofi Genzyme, Sarepta Therapeutics, Shire/Takeda, and TMA.
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Editor

Randolph W Evans MD

Dr. Evans of Baylor College of Medicine received honorariums from Abbvie, Amgen, Biohaven, Impel, Lilly, and Teva for speaking engagements.
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Former Authors

Glen H J Stevens MD
Asa J Wilbourn MD
Anil Nanda MD FACS
Peter C Shin MD
Vijay Kumar MD
Rajesh Acharya MD
Mark R Shaya MD
C Keilty Darnall MD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-10: Injury of other blood vessels at lower leg level: S85.8

Injury of tibial nerve at lower leg level: S84.0

Lesion of medial popliteal nerve: G57.4

Tarsal tunnel syndrome: G57.5
ICD-11: Injury of tibial nerve at lower leg level: NC94.0

Injury of other specified blood vessels at lower leg level: NC95.Y

Lesion of tibial nerve: 8C11.4

Tarsal tunnel syndrome: 8C11.5

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Tibial nerve injuries

Associated Disorders

Neurofibromatosis

Differential Diagnosis

partial sciatic nerve lesion
sacral plexopathy
S1 radiculopathies
S2 radiculopathies

Also Relevant

Peripheral nerve injuries
Peroneal neuropathy
Sciatic neuropathy

Tibial nerve injuries …

Tibial nerve injuries

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Third nerve palsy

Nystagmus

Neuropathies associated with cytomegalovirus infection

Brain death/death by neurologic criteria

Late-life migrainous accompaniments

Clinical evaluation of peripheral neuropathies

Hepatic encephalopathy

Cervical spondylotic myelopathy

Tibial nerve injuries

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Third nerve palsy

Nystagmus

Neuropathies associated with cytomegalovirus infection

Brain death/death by neurologic criteria

Late-life migrainous accompaniments

Clinical evaluation of peripheral neuropathies

Hepatic encephalopathy

Cervical spondylotic myelopathy

This is an article preview.
Start a Free Account
to access the full version.