Magnetic resonance imaging (MRI) and ultrasound are comparable in efficacy and helpful in diagnosis although both have a false positive rate of 15 - 20%. MRI can reliably detect most full-thickness tears although very small pinpoint tears may be missed. In such situations, an MRI combined with an injection of contrast material, an MR-arthrogram, may help to confirm the diagnosis. It should be realized that a normal MRI cannot fully rule out a small tear (a false negative) while partial-thickness tears are not as reliably detected. While MRI is sensitive in identifying tendon degeneration (tendinopathy), it may not reliably distinguish between a degenerative tendon and a partially torn tendon. Again, magnetic resonance arthrography can improve the differentiation. An overall sensitivity of 91% (9% false negative rate) has been reported indicating that magnetic resonance arthrography is reliable in the detection of partial-thickness rotator cuff tears. However, its routine use is not advised, since it involves entering the joint with a needle with potential risk of infection. Consequently, the test is reserved for cases in which the diagnosis remains unclear.

X-rays may help visualize bone spurs, acromial anatomy and arthritis. Further, calcification in the subacromial space and rotator cuff may be revealed. Osteoarthritis of the acromioclavicular (AC) joint may co-exist and is usually demonstrated on radiographs.

MRI imagining can reveal fluid accumulation in the bursa and assess adjacent structures. In chronic cases caused by impingement tendinosis and tears in the rotator cuff may be revealed. At US, an abnormal bursa may show (1) fluid distension, (2) synovial proliferation, and/or (3) thickening of the bursal walls. In any case, the magnitude of pathological findings does not correlate with the magnitude of the symptoms.

Impingement syndrome can usually be diagnosed by history and physical exam. On physical exam, the physician may twist or elevate the patient's arm to test for reproducible pain (Neer sign and Hawkins-Kennedy test). These tests help localize the pathology to the rotator cuff; however, they are not specific for impingement. Neer sign may also be seen with subacromial bursitis.

The physician may inject lidocaine (usually combined with a steroid) into the bursa, and if there is an improved range of motion and decrease in pain, this is considered a positive "Impingement Test". It not only supports the diagnosis for impingement syndrome, but it is also therapeutic.

Plain x-rays of the shoulder can be used to detect some joint pathology and variations in the bones, including acromioclavicular arthritis, variations in the acromion, and calcification. However, x-rays do not allow visualization of soft tissue and thus hold a low diagnostic value. Ultrasonography, arthrography and MRI can be used to detect rotator cuff muscle pathology. MRI is the best imaging test prior to arthroscopic surgery. Due to lack of understanding of the pathoaetiology, and lack of diagnostic accuracy in the assessment process by many physicians, several opinions are recommended before intervention.

Musculoskeletal ultrasound has been advocated by experienced practitioners, avoiding the radiation of X-ray and the expense of MRI while demonstrating comparable accuracy to MRI for identifying and measuring the size of full-thickness and partial-thickness rotator cuff tears. This modality can also reveal the presence of other conditions that may mimic rotator cuff tear at clinical examination, including tendinosis, calcific tendinitis, subacromial subdeltoid bursitis, greater tuberosity fracture, and adhesive capsulitis. However, MRI provides more information about adjacent structures in the shoulder such as the capsule, glenoid labrum muscles and bone and these factors should be considered in each case when selecting the appropriate study.

It is possible to prevent the onset of prepatellar bursitis, or prevent the symptoms from worsening, by avoiding trauma to the knee or frequent kneeling. Protective knee pads can also help prevent prepatellar bursitis for those whose professions require frequent kneeling and for athletes who play contact sports, such as American football, basketball, and wrestling.

In patients with bursitis who have rheumatoid arthritis, short term improvements are not taken as a sign of resolution and may require long term treatment to ensure recurrence is minimized. Joint contracture of the shoulder has also been found to be at a higher incidence in type two diabetics, which may lead to frozen shoulder (Donatelli, 2004).

The diagnosis of patellofemoral pain syndrome is made by ruling out patellar tendinitis, prepatellar bursitis, plica syndrome, Sinding-Larsen and Johansson syndrome, and Osgood–Schlatter disease.

Patients can be observed standing and walking to determine patellar alignment. The Q-angle, lateral hypermobility, and J-sign are commonly used determined to determine patellar maltracking. The patellofemoral glide, tilt, and grind tests (Clarke's sign), when performed, can provide strong evidence for PFPS. Lastly, lateral instability can be assessed via the patellar apprehension test, which is deemed positive when there is pain or discomfort associated with lateral translation of the patella.

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.

Imaging features of adhesive capsulitis are seen on non-contrast MRI, though MR arthrography and invasive arthroscopy are more accurate in diagnosis. Ultrasound and MRI can help in diagnosis by assessing the coracohumeral ligament, with a width of greater than 3 mm being 60% sensitive and 95% specific for the diagnosis. The condition can also be associated with edema or fluid at the rotator interval, a space in the shoulder joint normally containing fat between the supraspinatus and subscapularis tendons, medial to the rotator cuff. Shoulders with adhesive capsulitis also characteristically fibrose and thicken at the axillary pouch and rotator interval, best seen as dark signal on T1 sequences with edema and inflammation on T2 sequences. A finding on ultrasound associated with adhesive capsulitis is hypoechoic material surrounding the long head of the biceps tendon at the rotator interval, reflecting fibrosis. In the painful stage, such hypoechoic material may demonstrate increased vascularity with Doppler ultrasound.

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.

Diagnosis of tendinitis and bursitis begins with a medical history and physical examination. X rays do not show tendons or the bursae but may be helpful in ruling out bony abnormalities or arthritis. The doctor may remove and test fluid from the inflamed area to rule out infection.

Ultrasound scans are frequently used to confirm a suspected tendinitis or bursitis as well as rule out a tear in the rotator cuff muscles.

Impingement syndrome may be confirmed when injection of a small amount of anesthetic (lidocaine hydrochloride) into the space under the acromion relieves pain.

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.

Because wear on the hip joint traces to the structures that support it (the posture of the legs, and ultimately, the feet), proper fitting shoes with adequate support are important to preventing GTPS. For someone who has flat feet, wearing proper orthotic inserts and replacing them as often as recommended are also important preventive measures.

Strength in the core and legs is also important to posture, so physical training also helps to prevent GTPS. But it is equally important to avoid exercises that damage the hip.

There are several types of inflammation that can cause knee pain, including sprains, bursitis, and injuries to the meniscus. A diagnosis of prepatellar bursitis can be made based on a physical examination and the presence of risk factors in the person's medical history; swelling and tenderness at the front of the knee, combined with a profession that requires frequent kneeling, suggest prepatellar bursitis. Swelling of multiple joints along with restricted range of motion may indicate arthritis instead.

A physical examination and medical history are generally not enough to distinguish between infectious and non-infectious bursitis; aspiration of the bursal fluid is often required for this, along with a cell culture and Gram stain of the aspirated fluid. Septic prepatellar bursitis may be diagnosed if the fluid is found to have a neutrophil count above 1500 per microliter, a threshold significantly lower than that of septic arthritis (50,000 cells per microliter). A tuberculosis infection can be confirmed using a roentgenogram and urinalysis.

If severe pain persists after the first 24hours it is recommended that an individual consult with a professional who can make a diagnosis and implement a treatment plan so the patient can return to everyday activities (Flegel, 2004). These are some of the tools that a professional can use to help make a full diagnosis;

Nerve conduction studies may also be used to localize nerve dysfunction ("e.g.", carpal tunnel syndrome), assess severity, and help with prognosis.

Electrodiagnosis also helps differentiate between myopathy and neuropathy.

Ultimately, the best method of imaging soft tissue is magnetic resonance imaging (MRI), though it is cost-prohibitive and carries a high false positive rate.

The best diagnosis for a SLAP tear is a clinical exam

followed by an MRI combined with a contrast agent

To prevent the problem, a common recommendation is to keep the shoulder joint fully moving to prevent a frozen shoulder. Often a shoulder will hurt when it begins to freeze. Because pain discourages movement, further development of adhesions that restrict movement will occur unless the joint continues to move full range in all directions (adduction, abduction, flexion, rotation, and extension). Physical therapy and occupational therapy can help with continued movement.

If the knee is swollen and red and warm to the touch when compared to the other knee, a doctor may be concerned about inflammation due to rheumatoid arthritis or a crystalline arthritis, such as gout or pseudogout, or joint infection. Besides sending the joint fluid to a laboratory for analysis, blood tests may requested to determine a white blood cell count, erythrocyte sedimentation rate, and perhaps the level of C-reactive protein or uric acid. If blood tests reveal Lyme disease antibodies forming, the condition may be attributed to it.

A doctor may begin the diagnosis by asking the patient to stand on one leg and then the other, while observing the effect on the position of the hips. Palpating the hip and leg may reveal the location of the pain, and range-of-motion tests can help to identify its source.

X-rays, ultrasound and magnetic resonance imaging may reveal tears or swelling. But often these imaging tests do not reveal any obvious abnormality in patients with documented GTPS.

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.

An X-ray is useful to verify that there is no break or dislocation when there is a history of trauma. May show signs of osteoarthritis.

This condition is usually curable with appropriate treatment, or sometimes it heals spontaneously. If it is painless, there is little cause for concern.

Correcting any contributing biomechanical abnormalities and stretching tightened muscles, such as the iliopsoas muscle or iliotibial band, is the goal of treatment to prevent recurrence.

Referral to an appropriate professional for an accurate diagnosis is necessary if self treatment is not successful or the injury is interfering with normal activities. Medical treatment of the condition requires determination of the underlying pathology and tailoring therapy to the cause. The examiner may check muscle-tendon length and strength, perform joint mobility testing, and palpate the affected hip over the greater trochanter for lateral symptoms during an activity such as walking.

Impingement syndrome is usually treated conservatively, but sometimes it is treated with arthroscopic surgery or open surgery. Conservative treatment includes rest, cessation of painful activity, and physical therapy. Physical therapy treatments would typically focus at maintaining range of movement, improving posture, strengthening shoulder muscles, and reduction of pain. Physical therapists may employ the following treatment techniques to improve pain and function: joint mobilization, interferential therapy, accupuncture, soft tissue therapy, therapeutic taping, rotator cuff strengthening, and education regarding the cause and mechanism of the condition. NSAIDs and ice packs may be used for pain relief.

Therapeutic injections of corticosteroid and local anaesthetic may be used for persistent impingement syndrome. The total number of injections is generally limited to three due to possible side effects from the corticosteroid. A recent systematic review of level one evidence, showed corticoestroid injections only give small and transient pain relief.

A number of surgical interventions are available, depending on the nature and location of the pathology. Surgery may be done arthroscopically or as open surgery. The impinging structures may be removed in surgery, and the subacromial space may be widened by resection of the distal clavicle and excision of osteophytes on the under-surface of the acromioclavicular joint. Damaged rotator cuff muscles can be surgically repaired.

A self-treatment recommended by the U.S. Army for a soft tissue injury of the iliopsoas muscle treatment, like for other soft tissue injuries, is a HI-RICE (Hydration, Ibuprofen, Rest, Ice, Compression, Elevation) regimen lasting for at least 48 to 72 hours after the onset of pain. "Rest" includes such commonsense prescriptions as avoiding running or hiking (especially on hills), and avoiding exercises such as jumping jacks, sit-ups or leg lifts/flutter kicks.

Stretching of the tight structures (piriformis, hip abductor, and hip flexor muscle) may alleviate the symptoms. The involved muscle is stretched (for 30 seconds), repeated three times separated by 30 second to 1 minute rest periods, in sets performed two times daily for six to eight weeks. This should allow one to progress back into jogging until symptoms disappear.