Manual therapy and exercise have better efficacy in the long term than electrophysical agents and exercise for function, but not for pain. Manual therapy and exercise are preferably focused at stretching the plantar fascia.

Achilles tendinitis is mainly diagnosed by a medical history taking and a physical examination. Projectional radiography shows calcification deposits within the tendon at its calcaneal insertion in approximately 60 percent of cases. Magnetic resonance imaging (MRI) can determine the extent of tendon degeneration, and may show differential diagnoses such as bursitis.

The differential diagnosis for heel pain is extensive and includes pathological entities including, but not limited to the following: calcaneal stress fracture, calcaneal bursitis, osteoarthritis, spinal stenosis involving the nerve roots of lumbar spinal nerve 5 (L5) or sacral spinal nerve 1 (S1), calcaneal fat pad syndrome, hypothyroidism, seronegative spondyloparthopathies such as reactive arthritis, ankylosing spondylitis, or rheumatoid arthritis (more likely if pain is present in both heels), plantar fascia rupture, and compression neuropathies such as tarsal tunnel syndrome or impingement of the medial calcaneal nerve.

A determination about a diagnosis of plantar fasciitis can usually be made based on a person's medical history and physical examination. In cases in which the physician suspects fracture, infection, or some other serious underlying condition, an x-ray may be used to make a differential diagnosis. However, and especially for people who stand or walk a lot at work, x-rays should not be used to screen for plantar fasciitis unless imaging is otherwise indicated as using it outside of medical guidelines is unnecessary health care.

Plantar fasciitis is usually diagnosed by a health care provider after consideration of a person's presenting history, risk factors, and clinical examination. Tenderness to palpation along the inner aspect of the heel bone on the sole of the foot may be elicited during the physical examination. The foot may have limited dorsiflexion due to tightness of the calf muscles or the Achilles tendon. Dorsiflexion of the foot may elicit the pain due to stretching of the plantar fascia with this motion. Diagnostic imaging studies are not usually needed to diagnose plantar fasciitis. However, in certain cases a physician may decide imaging studies (such as X-rays, diagnostic ultrasound or MRI) are warranted to rule out serious causes of foot pain.

Other diagnoses that are typically considered include fractures, tumors, or systemic disease if plantar fasciitis pain fails to respond appropriately to conservative medical treatments. Bilateral heel pain or heel pain in the context of a systemic illness may indicate a need for a more in-depth diagnostic investigation. Under these circumstances, diagnostic tests such as a CBC or serological markers of inflammation, infection, or autoimmune disease such as C-reactive protein, erythrocyte sedimentation rate, anti-nuclear antibodies, rheumatoid factor, HLA-B27, uric acid, or Lyme disease antibodies may also be obtained. Neurological deficits may prompt an investigation with electromyography to evaluate for damage to the nerves or muscles.

An incidental finding associated with this condition is a heel spur, a small bony calcification on the calcaneus (heel bone), which can be found in up to 50% of those with plantar fasciitis. In such cases, it is the underlying plantar fasciitis that produces the heel pain, and not the spur itself. The condition is responsible for the creation of the spur though the clinical significance of heel spurs in plantar fasciitis remains unclear.

As stated earlier, musculoskeletal disorders can cost up to $15–$20 billion in direct costs or $45–$55 billion in indirect expenses. This is about $135 million a day Tests that confirm or correct TTS require expensive treatment options like x-rays, CT-scans, MRI and surgery. 3 former options for TTS detect and locate, while the latter is a form of treatment to decompress tibial nerve pressure Since surgery is the most common form of TTS treatment, high financial burden is placed upon those diagnosed with the rare syndrome.

Though a neuroma is a soft tissue abnormality and will not be visualized on standard radiographs, the first step in the assessment of forefoot pain is an X-ray in order to evaluate for the presence of arthritis and exclude stress fractures/reactions and focal bone lesions, which may mimic the symptoms of a neuroma. Ultrasound (sonography) accurately demonstrates thickening of the interdigital nerve within the web space of greater than 3mm, diagnostic of a Morton’s neuroma. This typically occurs at the level of the intermetatarsal ligament. Frequently, intermetatarsal bursitis coexists with the diagnosis. Other conditions that may also be visualized with ultrasound and can be clinically confused with a neuroma include synovitis/capsulitis from the adjacent metatarsophalangeal joint, stress fractures/reaction, and plantar plate disruption. MRI can similarly demonstrate the above conditions; however, in the setting where more than one abnormality coexists, ultrasound has the added advantage of determining which may be the source of the patient’s pain by applying direct pressure with the probe. Further to this, ultrasound can be used to guide treatment such as cortisone injections into the webspace, as well as alcohol ablation of the nerve.

It is important to differentiate between infected and non-infected bursitis. People may have surrounding cellulitis and systemic symptoms include a fever. The bursa should be aspirated to rule out an infectious process.

Bursae that are not infected can be treated symptomatically with rest, ice, elevation, physiotherapy, anti-inflammatory drugs and pain medication. Since bursitis is caused by increased friction from the adjacent structures, a compression bandage is not suggested because compression would create more friction around the joint. Chronic bursitis can be amenable to bursectomy and aspiration.

Bursae that are infected require further investigation and antibiotic therapy. Steroid therapy may also be considered. In cases when all conservative treatment fails, surgical therapy may be necessary. In a bursectomy the bursa is cut out either endoscopically or with open surgery. The bursa grows back in place after a couple of weeks but without any inflammatory component.

The main differential diagnosis of heel pad syndrome is plantar fasciitis. In heel pad syndrome all parts of the heel are tender while in plantar fasciitis typically only the part of the heel closer to the toes is sore.

Diagnosis is based upon physical examination findings. Patients' pain history and a positive Tinel's sign are the first steps in evaluating the possibility of tarsal tunnel syndrome. X-ray can rule out fracture. MRI can assess for space occupying lesions or other causes of nerve compression. Ultrasound can assess for synovitis or ganglia. Nerve conduction studies alone are not, but they may be used to confirm the suspected clinical diagnosis. Common causes include trauma, varicose veins, neuropathy and space-occupying anomalies within the tarsal tunnel. Tarsal tunnel syndrome is also known to affect both athletes and individuals that stand a lot.

A Neurologist or a Physiatrist usually administers nerve conduction tests or supervises a trained technologist. During this test, electrodes are placed at various spots along the nerves in the legs and feet. Both sensory and motor nerves are tested at different locations. Electrical impulses are sent through the nerve and the speed and intensity at which they travel is measured. If there is compression in the tunnel, this can be confirmed and pinpointed with this test. Some doctors do not feel that this test is necessarily a reliable way to rule out TTS. Some research indicates that nerve conduction tests will be normal in at least 50% of the cases.

Given the unclear role of electrodiagnostics in the diagnosis of tarsal tunnel syndrome, efforts have been made in the medical literature to determine which nerve conduction studies are most sensitive and specific for tibial mononeuropathy at the level of the tarsal tunnel. An evidence-based practice topic put forth by the professional organization, the American Association of Neuromuscular & Electrodiagnostic Medicine has determined that Level C, Class III evidence exists for the use of tibial motor nerve conduction studies, medial and lateral plantar mixed nerve conduction studies, and medial and lateral plantar sensory nerve conduction studies. The role of needle electromyography remains less defined.

Tarsal Tunnel Syndrome (TTS) is most closely related to Carpal Tunnel Syndrome (CTS). However, the commonality to its counterpart is much less or even rare in prevalence Studies have found that patients with rheumatoid arthritis (RA) show signs of distal limb neuropathy. The posterior tibial nerve serves victim to peripheral neuropathy and often show signs of TTS amongst RA patients. Therefore, TTS is a common discovery found in the autoimmune disorder of rheumatoid arthritis

Ankle sprains can occur through either sports or activities of daily living, and individuals can be at higher or lower risk depending on a variety of circumstances including their homeland, race, age, sex, or profession In addition, there are different types of ankle sprains such as eversion ankle sprains and inversion ankle sprains. Overall, the most common type of ankle sprain to occur is an inversion ankle sprain, where excessive plantar flexion and supination cause the anterior talofibular ligament to be affected. A study showed that for a population of Scandinavians, inversion ankle sprains accounted for 85% of all ankle sprains Most ankle sprains occur in more active people, such as athletes and regular exercisers.

Most people improve significantly in the first two weeks. However, some still have problems with pain and instability after one year (5–30%). Re-injury is also very common.

Deteriorating changes start to appear with age, but attempting to slow down these changes is key in the prevention of Achilles tendinitis. Performing consistent physical activity will improve the elasticity and strength of the tendon, which will assist in resisting the forces that are applied.

It is essential to stretch and warm-up before beginning an exercise session in order to prepare and protect the tendon for work. Warm-ups enhance the tendon's capability of being stretched, further aiding in protection from injury. Prevention of recurrence includes following appropriate exercise habits and wearing low-heeled shoes. In the case of incorrect foot alignment, orthotics can be used as a preventative way to properly position the feet. Footwear that is specialized to provide shock-absorption can be utilized to defend the longevity of the tendon. Achilles tendon injuries can be the result of exceeding the tendon's capabilities for loading, therefore it is important to gradually adapt to exercise if someone is inexperienced, sedentary, or is an athlete who is not progressing at a steady rate.

Preventive exercises are aimed at strengthening the gastrocnemius and soleus muscles, typically by eccentric strengthening exercises. This eccentric training method is especially important for individuals with chronic Achilles tendinosis which is classified as the degeneration of collagen fibers. Eccentric exercises improve the tensile strength of the tendon and lengthen the muscle-tendon junction, decreasing the amount of strain experienced with ankle joint movements. These involve repetitions of slowly raising and lowering the body while standing on the affected leg, using the opposite arm to assist balance and support if necessary, and starting with the heel in a hyperextended position. (Hyperextension is typically achieved by balancing the forefoot on the edge of a step, a thick book, or a barbell weight. so that the point of the heel is a couple of inches below the forefoot.)

Non-specific treatments include:

- Non-steroidal anti-inflammatory drugs (NSAIDs): ibuprofen, naproxen or aspirin

- Heat or ice

- A counter-force brace or "elbow strap" to reduce strain at the elbow epicondyle, to limit pain provocation and to protect against further damage.

Before anesthetics and steroids are used, conservative treatment with an occupational therapist may be attempted. Before therapy can commence, treatment such as the common rest, ice, compression and elevation (R.I.C.E.) will typically be used. This will help to decrease the pain and inflammation; rest will alleviate discomfort because golfer's elbow is an overuse injury. The patient can use a tennis elbow splint for compression. A pad can be placed anteromedially on the proximal forearm. The splint is made in 30–45 degrees of elbow flexion. A daytime elbow pad also may be useful, by limiting additional trauma to the nerve.

Therapy will include a variety of exercises for muscle/tendon reconditioning, starting with stretching and gradual strengthening of the flexor-pronator muscles. Strengthening will slowly begin with isometrics and progresses to eccentric exercises helping to extend the range of motion back to where it once was. After the strengthening exercises, it is common for the patient to ice the area.

Simple analgesic medication has a place, as does more specific treatment with oral anti-inflammatory medications (NSAIDs). These will help control pain and any inflammation. A more invasive treatment is the injection into and around the inflamed and tender area of a long-acting glucocorticoid (steroid) agent. After causing an initial exacerbation of symptoms lasting 24 to 48 hours, this may produce an improvement of the condition in some five to seven days.

The ulnar nerve runs in the groove between the medial humeral epicondyle and the olecranon process of the ulna. It is most important that this nerve should not be damaged accidentally in the process of injecting a golfer's elbow.

If all else fails, epicondylar debridement (a surgery) may be effective. The ulnar nerve may also be decompressed surgically.

If the appropriate remediation steps are taken - rest, ice, and rehabilitative exercise and stretching - recovery may follow. Few patients will need to progress to steroid injection, and less than 10% will require surgical intervention.

With rest and quadriceps flexibility exercises the condition settles with no secondary disability. Sometimes, if the condition does not settle, calcification appears in the ligament. This condition is comparable to Osgood-Schlatter’s disease and usually recovers spontaneously. If rest fails to provide relief, the abnormal area is removed and the paratenon is stripped.

Conventional radiography is usually the initial assessment tool when a calcaneal fracture is suspected. Recommended x-ray views are (a) axial, (b) anteroposterior, (c) oblique and (d) views with dorsiflexion and internal rotation of the foot. However, conventional radiography is limited for visualization of calcaneal anatomy, especially at the subtalar joint. A CT scan is currently the imaging study of choice for evaluating calcaneal injury and has substituted conventional radiography in the classification of calcaneal fractures. Axial and coronal views are obtained for proper visualization of the calcaneus, subtalar, calcaneocuboid and talonavicular joints.

It is often seen as a repetitive stress injury, and thus lifestyle modification is typically the basic course of management strategies. For example, a person should begin doing foot and calf workouts. Strong muscles in the calves and lower legs will help take the stress off the bone and thus help cure or prevent heel spurs. Icing the area is an effective way to get immediate pain relief.

Initial diagnosis often is made during routine physical examination. Such diagnosis can be confirmed by a medical professional such as a neurologist, orthopedic surgeon or neurosurgeon. A person with foot drop will have difficulty walking on his or her heels because he will be unable to lift the front of the foot (balls and toes) off the ground. Therefore, a simple test of asking the patient to dorsiflex may determine diagnosis of the problem. This is measured on a 0-5 scale that observes mobility. The lowest point, 0, will determine complete paralysis and the highest point, 5, will determine complete mobility.

There are other tests that may help determine the underlying etiology for this diagnosis. Such tests may include MRI, MRN, or EMG to assess the surrounding areas of damaged nerves and the damaged nerves themselves, respectively. The nerve that communicates to the muscles that lift the foot is the peroneal nerve. This nerve innervates the anterior muscles of the leg that are used during dorsi flexion of the ankle. The muscles that are used in plantar flexion are innervated by the tibial nerve and often develop tightness in the presence of foot drop. The muscles that keep the ankle from supination (as from an ankle sprain) are also innervated by the peroneal nerve, and it is not uncommon to find weakness in this area as well. Paraesthesia in the lower leg, particularly on the top of the foot and ankle, also can accompany foot drop, although it is not in all instances.

A common yoga kneeling exercise, the Varjrasana has, under the name "yoga foot drop," been linked to foot drop.

The issue of hoof care is a subject of great debate. Corrective shoeing can be beneficial to horses suffering from navicular disease, although sometimes the effects are only temporary. Others believe that removing the shoes altogether is the best way to manage this disease, as it allows increased circulation to the hoof. People on both sides agree that proper hoof shape and angle are an important long-term management plan for a horse with navicular disease. As with laminitis, different horses may respond in different ways to a given technique, so the farrier, owner, and veterinarian should work as a team to formulate a plan and to adapt if the initial plan is not effective.

People who choose to treat navicular disease through shoeing may use a shoe designed to lift and support the heels. This can sometimes be accomplished with a flat shoe and trimming alone. Wedge pads or wedged shoes are often used, but can amplify heel-related problems if present. Another strategy is to use a bar type shoe. Often, an egg-bar shoe, or straight bar shoe. Some horses benefit from shoes that change the breakover of their foot (like a rolled toe). With or without shoes, the hoof must be trimmed in such a way as to restore the balance and angle that may have been lost. Horses with long toe-low heel conformation need careful trimming to counter this. Horses with upright feet may need their heels lowered and a shoe that will allow their heels to spread. Early intervention is key; in one study, shoeing was successful in 97% of horses treated within ten months of the onset of signs, while only 54% of horses lame for over a year responded.

Advocates of barefoot trimming cite recent studies which show that removing the shoes can help alleviate the symptoms of navicular disease, and in some cases, reverse some of the damage done to the hoof. Because navicular disease can be caused, or at least exacerbated by shoeing, removing the cause is the first step in this strategy toward the management of pain in the animal. Successive carefully applied trims help to restore the natural angle and shape of the hoof, while walking helps to stimulate circulation to the hoof. It is not uncommon to find horses whose navicular disease is completely manageable through corrective barefoot trimming. However, this may require a transition period lasting from weeks to years where the horse may remain lame, or may never become sound.

If there is significant degeneration in the bone, a flexor cortex cyst, adhesions to the deep digital flexor tendon, or avulsion fractures, relief is typically incomplete no matter what foot care technique is used.

Putting the foot into proper neurological and biomechanical balance is crucial. Often navicular horses have long toes and underrun heels with very little inner wall depth or strength. Exposing the horse to proper stimulus to improve hoof form and structure is also vital.

The most common treatment for discrepancies in leg length is the use of a simple heel lift, which can be placed within the shoe. In cases where the length discrepancy is moderate, an external build up to the shoe is usually more comfortable. In severe cases, surgery can be used to make the longer leg shorter (or impede its growth), and/or make the shorter leg longer.

Although prone "functional leg length" is a widely used chiropractic tool in their Activator technique, it is not a recognized anthropometric technique, since legs are usually of unequal length, and measurements in the prone position are not entirely valid estimates of standing X-ray differences. Measurements in the standing position are far more reliable. Another confounding factor is that simply moving the two legs held together and leaning them imperceptibly to one side or the other produces different results.

Clinical measurement of leg length conventionally uses the distance from the anterior superior iliac spine to the medial malleolus. Projectional radiographic measurements of leg length have two main variants:

- Teleroentgenogram, which projects the entirety of both legs at the same time.

- Orthoroentgenogram, which takes separate images of the hip, knee and ankle.

On X-rays, the length of the lower limb can be measured from the proximal end of femoral head to the center of the plafond of the distal tibia.

There can be several concurrent causes. Trauma, auto-immune disorders, infection and iatrogenic (medicine-related) factors can all cause bursitis. Bursitis is commonly caused by repetitive movement and excessive pressure. Shoulders, elbows and knees are the most commonly affected. Inflammation of the bursae may also be caused by other inflammatory conditions such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus and gout. Immune deficiencies, including HIV and diabetes, can also cause bursitis. Infrequently, scoliosis can cause bursitis of the shoulders; however, shoulder bursitis is more commonly caused by overuse of the shoulder joint and related muscles.

Traumatic injury is another cause of bursitis. The inflammation irritates because the bursa no longer fits in the original small area between the bone and the functionary muscle or tendon. When the bone increases pressure upon the bursa, bursitis results. Sometimes the cause is unknown. It can also be associated with various other chronic systemic diseases.

Aside from surgery, there are a few options for handling an accessory navicular bone that has become symptomatic. This includes immobilization, icing, medicating, physical therapy, and orthotic devices. Immobilizing involves placing the foot and ankle in a cast or removable walking boot. This alleviates stressors on the foot and can decrease inflammation. Icing will help reduce swelling and inflammation. Medication involves usage of nonsteroidal anti-inflammatory drugs, or steroids (taken orally or injected) to decrease inflammation. Physical therapy can be prescribed in order to strengthen the muscles and help decrease inflammation. Physical therapy can also help prevent the symptoms from returning. Orthotic devices (arch support devices that fit in a shoe) can help prevent future symptoms. Occasionally, the orthotic device will dig into the edge of the accessory navicular and cause discomfort. For this reason, the orthotic devices made for the patient should be carefully constructed.

The condition is usually seen in athletic individuals typically between 10–14 years of age. Following a strain or partial rupture of patellar ligament the patient develops a traction ‘tendinitis’ characterized by pain and point tenderness at the inferior (lower) pole of the patella associated with focal swelling.

Children with cerebral palsy are particularly prone to SLJ 4.

In medicine, an enthesopathy refers to a disorder involving the attachment of a tendon or ligament to a bone. This site of attachment is known as the entheses.

If the condition is known to be inflammatory, it can more precisely be called an enthesitis.