Nov. 27, 2022
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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 (28). 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.
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