This article includes discussion of ulnar neuropathies, Guyon canal neuropathy, ulnar neuropathy at the wrist, and flexor carpi ulnaris exit compression.
Jun. 07, 2021
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This article includes discussion of tibial nerve injuries and Morton neuroma. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
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 (25), and a host of rare and unusual causes including posterior tibial nerve impingement from a tibial spine fixation screw (20). 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 (22).
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. 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 on various areas on the sole of the foot depending on the particular terminal nerve involved. If there is sensory loss on the heel, usually the medial calcaneal sensory branch is involved, localizing the lesion to 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 currently 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 (27). Interestingly, 7 cases were associated with an autoimmune disorder such as Sjogren syndrome, rheumatoid arthritis, psoriasis, cryoglobulinemia, nonsystemic vasculitic neuropathy, or histiocytic vasculitis, and 2 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.
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.
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 1 month after the interventional procedure. At that time, examination disclosed obvious atrophy of the right calf muscles.
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 boarder 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 recording abductor digiti quinti pedis, and low in amplitude recording abductor hallucis. 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.
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 distal third of the thigh. With the common peroneal nerve, the other derivative of the sciatic nerve, it lies deep to 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 (21). 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.
Tibial nerve entrapment is most common in the tarsal tunnel. Tarsal tunnel syndrome is, however, very rare.
Most causes of tibial neuropathies are not preventable by any specific action that can be easily predicted. Common sense is the best advice. Proper shoe fitting and care with avoidance of compression is important. There was a case report of a hockey player in Canada who suffered from a neuropathy due to an inflatable hockey skate; the patient improved clinically after discontinuing use of the skate (26).
The differential diagnosis of tibial neuropathy includes a partial sciatic nerve lesion, sacral plexopathy, and S1 or S2 radiculopathies. Extensive investigations of more proximal muscle groups, especially gluteal and hamstrings, may be helpful.
In a retrospective chart review of 109 patients with electrodiagnostically confirmed sciatic neuropathies, a third of the cases were related to hip replacement surgery and less than 10% were due to inflammatory sciatic neuropathy (04). The electrophysiology demonstrated mostly axonal pathophysiology that in 5.5% of cases was predominantly in the tibial division. Favorable outcome was associated with young age, lack of severe initial weakness, and presence of tibial compound muscle action potential or sural sensory nerve action potential.
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 9 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) has 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 the assessment of peripheral nerve infiltration by malignant tumors, but more studies are needed (12).
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 8 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 6 of 8 patients. A more extensive surgery may be needed to effectively decompress the tibial nerve and its branches in tarsal tunnel syndrome (23). In addition to roof incision, this involves decompression of the medial plantar and lateral plantar nerves and the excision of the inter-tunnel septum.
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). 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 (24). 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 4 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 of patients with Morton neuroma. More recently, 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).
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 honorariums from ArgenX, Cello, Corbus, EcoR1, Momenta, NuFactor, Octapharma, Orphazyme, RA Pharma/UCB Biopharma, RMS Medical, Sanofi Genzyme, Shire/Takeda, Spark Therapeutics, and Third Rock for consulting work; and research or education grants from Alexion, Alnylam, Amicus, Biomarin, Briston Myers Squibb, Catalyst, Corbus, CSL Behring, FDA/OOPD, Genentech, Genetech, Grifols, GSK, Kezar, MDA, Mitsubishi Tanabe Pharma, Novartis, Octapharma, Orphazyme, Ra Pharma/UCB Biopharma, Sanofi Genzyme, Sarepta Therapeutics, Shire/Takeda, Spark Therapeutics, TMA, and Viromed.See Profile
Randolph W Evans MD
Dr. Evans of Baylor College of Medicine received honorariums from Allergan, Amgen and Novartis, Biohaven, Lilly, and Teva for speaking engagements.See Profile
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