Plantar canal syndrome

　　1. Causes of the disease

　　1. Congenital factors:Abnormal enlargement of the abductor hallucis, accessory abductor hallucis, calcaneal varus deformity, and flat feet can all reduce the practical volume of the plantar canal, thereby causing compression of the tibial nerve.

　　4. Fractures of the calcaneus and ankle:Poor reduction or malunion can also reduce the volume of the plantar canal. Moreover, an irregular base of the plantar canal can cause compression and friction, potentially injuring the tibial nerve.

　　3. Chronic injury:Occupational activities involving intense physical labor, long-distance runners, and individuals with frequent high-intensity plantar flexion and dorsiflexion of the ankle joint can lead to increased tendon gliding and enhanced friction, which may cause tenosynovitis, congestion, and edema of the sheath, as well as thickening of the flexor retinaculum. This can reduce the elasticity of the plantar canal, increase internal pressure, and compress the tibial nerve, affecting its blood supply and leading to neurological dysfunction. Additionally, patients with rheumatoid arthritis, osteoarthritis in the elderly, and other conditions may develop proliferative osteophytes, and osteophytes protruding into the plantar canal can also compress the tibial nerve.

　　4, Internal factors of the plantar canal:Bursitis, lipoma, varicose veins can also cause compression of the tibial nerve.

　　5, Others:Conditions such as hypothyroidism, pregnancy, varicose veins of the great saphenous vein and small saphenous vein, etc.

　　Second, pathogenesis

　　The most narrow part of the plantar canal is at its distal end, where all the nerve branches pass through and cross the fibrous holes at the origin of the abductor muscles before entering the sole of the foot. The medial nerve canal of the sole has the calcaneocuboid ligament as its superior margin, and the lateral nerve canal is surrounded by the plantar muscles, so external rotation and abduction of the foot can pull on the retinaculae and the abductor muscles, causing the plantar medial nerve and blood vessels to twist and compress, leading to symptoms of nerve compression. In addition, when the ankle joint is dorsiflexed or plantarflexed, the flexor retinaculum plays a restrictive role at the plantar canal, preventing the dislocation of tendons. If there is a sudden increase in the activity of the foot and ankle, an increase in tendon sliding and friction can cause tenosynovitis. If the activity of the foot and ankle continues to increase, the tenosynovium becomes increasingly congested and swollen, the flexor retinaculum thickens accordingly, the flexibility of the plantar canal decreases, and the pressure inside the plantar canal increases, which can compress the tibial nerve, affecting its blood supply and causing dysfunction of the nerve.

　　First, nerve compression:Changes in nerve function are proportional to the degree and duration of nerve compression. Repeated temporary ischemia in the early stages can produce pain and sensory abnormalities. Long-term nerve compression can lead to demyelination and nerve degeneration, with symptoms such as numbness, muscle weakness and atrophy, and prolonged nerve conduction time in the foot.

　　Second, pathological changes

　　1, Nerve compression exists at the fibrous origin of the flexor muscles, retinaculae, and the abductor muscle of the great toe.

　　2, Thickening of the tendinous synovium is seen in patients with rheumatoid arthritis.

　　In patients with fracture-related plantar fasciitis, nerve compression caused by post-traumatic fibrosis due to fractures can be found.

　　The onset of the disease is gradual, mostly occurring on one side. In the early stages, it presents as intermittent pain, tightness, swelling, discomfort, or numbness in the sole and heel of the foot. Sometimes the pain radiates to the lower leg, and sometimes there are cramps along the arch of the foot. The symptoms worsen after prolonged standing or walking, and there is a history of pain waking up at night. Most patients can alleviate the pain after taking off their shoes. As the condition progresses, the pain often gradually worsens, and further symptoms may include a decrease or loss of sensation in the area of the foot controlled by the tibial nerve, normal skin sensation at the heel, which is due to the plantar medial nerve branching off from the tibial nerve above the metatarsal bone or because the compressive site is below the plantar canal. In the late stage, signs of autonomic nervous system dysfunction may appear, such as shiny skin on the toes, hair loss, hypohidrosis, and even atrophy of the intrinsic muscles of the foot. The disappearance of the ability to distinguish between two points at a distance is an important indicator for early diagnosis; the Tinel sign posterior and inferior to the medial malleolus is often positive; pain can be induced by external rotation and abduction of the foot.

　　The most narrow part of the plantar canal is at its distal end, where all the nerve branches pass through and cross the fibrous holes at the origin of the abductor muscles before entering the sole of the foot.

　　Foot valgus can pull the retinaculum and the extensor digitorum brevis muscle to twist and compress the plantar medial nerve and blood vessels, making it easy to have symptoms of nerve compression. In addition, when the ankle joint is plantarflexed or dorsiflexed, the flexor retinaculum plays a constraint role at the plantar tunnel, preventing the tendons from slipping. If the activity of the foot and ankle increases abruptly, the tendons slide more, and friction increases, which can cause tendinitis. If the activity of the foot and ankle continues to increase, the synovial membrane becomes more and more congested and swollen, the flexor retinaculum also becomes thicker, the elasticity of the plantar tunnel decreases, and the pressure inside the plantar tunnel increases, which can compress the tibial nerve, affect its blood supply, and cause dysfunction of the nerve.

　　Avoid the above insufficient factors to prevent this disease!

　　1. EMG examination:It can be seen that the conduction speed of the plantar nerves on both sides of the sole is slow, and the latent period is prolonged.

　　2. X-ray examination:Can detect and understand the healing condition of the ankle joint and calcaneal fracture.

　　3. CT examination:Bilateral comparison can help identify cysts and tumors in the plantar tunnel.

　　This disease is mainly caused by various different tissue lesions that cause nerve compression. While undergoing active treatments such as surgery, reasonable dietary therapy should be carried out to help the recovery of nerve function. Focus on choosing diets rich in vitamin B1, vitamin B12, and niacin. In animal proteins such as liver, kidney, meat, dairy products, fish, shellfish, and egg foods, vitamin B12 is relatively high, which can be eaten more, and it is of great significance for the recovery of nerves.

　　I. Treatment

　　1. Conservative Treatment:For those with mild symptoms and in the early stage of onset, anti-inflammatory and analgesic drugs, rest, and intraplantar prednisolone infiltration can be given. The use of braces to maintain the foot in an inverted position can relax the flexor retinaculum, enlarge the plantar tunnel, and relieve pain.

　　2. Surgical Treatment:For those who are ineffective to conservative treatment and have obvious symptoms of nerve compression, a plantar tunnel decompression operation can be performed. In addition to releasing the flexor retinaculum, the plantar nerves on both sides also need to be released to the point where they enter the nerve canal, and the fibrous entrance of the nerve entrance needs to be incised.

　　II. Prognosis

　　The prognosis is still good after treatment.