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.

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.

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.

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).

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.

Diagnosis is made almost exclusively by history and physical examination alone. More than one finger may be affected at a time, though it usually affects the index, thumb, middle, or ring finger. The triggering is usually more pronounced late at night and into the morning, or while gripping an object firmly.

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

The diagnosis of the cause of a limp is often made based on history, physical exam findings, laboratory tests, and radiological examination. If a limp is associated with pain it should be urgently investigated, while non-painful limps can be approached and investigated more gradually. Young children have difficulty determining the location of leg pain, thus in this population, "knee pain equals hip pain". SCFE can usually be excluded by an x-ray of the hips. A ultrasound or x-ray guided aspiration of the hip joint maybe required to rule out an infectious process within the hip.

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.

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.

The natural history of disease for trigger finger remains uncertain.

There is some evidence that idiopathic trigger finger behaves differently in people with diabetes.

Recurrent triggering is unusual after successful injection and rare after successful surgery.

While difficulty extending the proximal interphalangeal joint may persist for months, it benefits from exercises to stretch the finger straighter.

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.

This test can see various warning signs that predict if OSD might occur. Ultrasonography can detect if there is any swelling within the tissue as well as cartilage swelling. Ultrasonography's main goal is to identify OSD in the early stage rather than later on. It has unique features such as detection of an increase of swelling within the tibia or the cartilage surrounding the area and can also see if there is any new bone starting to build up around the tibial tuberosity.

OSD may result in an avulsion fracture, with the tibial tuberosity separating from the tibia (usually remaining connected to a tendon or ligament). This injury is uncommon because there are mechanisms that prevent strong muscles from doing damage. The fracture on the tibial tuberosity can be a complete or incomplete break.

Type I: A small fragment is displaced proximally and does not require surgery.

Type II: The articular surface of the tibia remains intact and the fracture occurs at the junction where the secondary center of ossification and the proximal tibial epiphysis come together (may or may not require surgery).

Type III: Complete fracture (through articular surface) including high chance of meniscal damage. This type of fracture usually requires surgery.

X-ray of the affected wrist is required if a fracture is suspected. Anteroposterior (AP), lateral, and oblique views can be used together to describe the fracture. X-ray of the uninjured wrist should also be taken to determine if there are any normal anatomic variations. Investigation of a potential distal radial fracture includes assessment of the angle of the joint surface on lateral X-ray (volar/dorsal tilt), the loss of length of the radius from the collapse of the fracture (radial length), and congruency of the distal radioulnar joint (DRUJ). Displacement of the articular surface is the most important factor affecting prognosis and treatment. CT scan is often performed to further investigate the articular anatomy of the fracture, especially if surgery is considered. MRI can be considered to evaluate for soft tissue injuries, including damage to the TFCC and the interosseous ligaments.

PNE can be caused by pregnancy, scarring due to surgery, accidents and surgical mishaps. Anatomic abnormalities can result in PNE due to the pudendal nerve being fused to different parts of the anatomy, or trapped between the sacrotuberous and sacrospinalis ligaments. Heavy and prolonged bicycling, especially if an inappropriately shaped or incorrectly positioned bicycle seat is used, may eventually thicken the sacrotuberous and/or sacrospinous ligaments and trap the nerve between them, resulting in PNE.

Diagnosis may be evident clinically when the distal radius is deformed but should be confirmed by X-ray.

The differential diagnosis includes scaphoid fractures and wrist dislocations, which can also co-exist with a distal radius fracture. Occasionally, fractures may not be seen on X-rays immediately after the injury. Delayed X-rays, X-ray computed tomography (CT scan), or Magnetic resonance imaging (MRI) will confirm the diagnosis.

Typically, radiographs are taken of the hip from the front (AP view), and side (lateral view). Frog leg views are to be avoided, as they may cause severe pain and further displace the fracture. In situations where a hip fracture is suspected but not obvious on x-ray, an MRI is the next test of choice. If an MRI is not available or the patient can not be placed into the scanner a CT may be used as a substitute. MRI sensitivity for radiographically occult fracture is greater than CT. Bone scan is another useful alternative however substantial drawbacks include decreased sensitivity, early false negative results, and decreased conspicuity of findings due to age related metabolic changes in the elderly.

As the patients most often require an operation, full pre-operative general investigation is required. This would normally include blood tests, ECG and chest x-ray.

Similar to a tinel sign digital palpitation of the ischial spine may produce pain. In contrast, patients may report temporary relief with a diagnostic pudendal nerve block (see Injections), typically infiltrated near the ischial spine.

Electromyography can be used to measure motor latency along the pudendal nerve. A greater than normal conduction delay can indicate entrapment of the nerve.

Imaging studies using MR neurography may be useful. In patients with unilateral pudendal entrapment in the Alcock's canal, it is typical to see asymmetric swelling and hyperintensity affecting the pudendal neurovascular bundle.

In most people, ligaments (which are the tissues that connect bones to each other) are naturally tight in such a way that the joints are restricted to 'normal' ranges of motion. This creates normal joint stability. If muscular control does not compensate for ligamentous laxity, joint instability may result. The trait is almost certainly hereditary, and is usually something the affected person would just be aware of, rather than a serious medical condition. However, if there is widespread laxity of other connective tissue, then this may be a sign of Ehlers-Danlos syndrome.

Ligamentous laxity may also result from injury, such as from a vehicle accident. It can result from whiplash and be overlooked for years by doctors who are not looking for it, despite the chronic pain that accompanies the resultant spinal instability. Ligamentous laxity will show up on an upright magnetic resonance imaging (MRI), the only kind of MRI that will show soft tissue damage. It can be seen in standing stress radiographs in flexion, extension, and neutral views as well, and also digital motion X-ray, or DMX.

An advantage to having lax ligaments and joints is the ability to withstand pain from hyperextension; however, this is also a disadvantage as a lack of perceived pain can prevent a person from removing the ligament from insult, leading to ligament damage. This can also lead to death if you tear the wrong ligament. People with hypermobile joints (or "double-jointed" people), almost by definition, have lax ligaments.

Those who have loose ligaments in the legs and feet often mistakenly assume that they have flat feet. While their feet have an arch when not supporting weight, when stood upon, the arch will flatten. This is because the loose ligaments cannot support the arch in the way that they should. This can make walking and standing painful and tiring.

Pain will usually occur in the feet and lower legs, but can also spread to the back due to abnormal standing and walking habits. Wearing shoes that have good arch support can help minimize the discomfort. The underlying problem, however, is not solved by wearing shoes with arch supports or worsened by wearing shoes without arch support. There is currently no cure for the condition.

In addition, people with ligamentous laxity often have clumsy or deliberate gaits, owing to the body having to overcompensate for the greater amount of energy required to offset the weakened ligaments. The feet may be spread apart at a wide angle, and the knees may flex backwards slightly after each stride.

Those who have this disease may experience sprained ankles more frequently than other people.

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.

A limp at one hospital emergency department was the presenting complaint in 4% of children. It occurs twice as commonly in boys as in girls.

X-rays of the affected hip usually make the diagnosis obvious; AP (anteroposterior) and lateral views should be obtained.

Trochanteric fractures are subdivided into either intertrochanteric (between the greater and lesser trochanter) or pertrochanteric (through the trochanters) by the Müller AO Classification of fractures. Practically, the difference between these types is minor. The terms are often used synonymously. An "isolated trochanteric fracture" involves one of the trochanters without going through the anatomical axis of the femur, and may occur in young individuals due to forceful muscle contraction. Yet, an "isolated trochanteric fracture" may not be regarded as a true hip fracture because it is not cross-sectional.

In order to qualify a patient's condition as BSS, the bending angle must be greater than 45 degrees. While the presence of the condition is very easy to note, the cause of the condition is much more difficult to discern. Conditions not considered to be BSS include vertebral fractures, previously existing conditions, and ankylosing spondylitis. Lower-back CT scans and MRIs can typically be used to visualize the cause of the disease. Further identification of the cause can be done by histochemical or cellular analysis of muscle biopsy.

Camptocormia is becoming progressively found in patients with Parkinson's disease.

The diagnosis of Parkinson's-associated camptocormia includes the use of imaging of the brain and the spinal cord, along with electromyography or muscle biopsies.

Muscle biopsies are also a useful tool to diagnose camptocormia. Muscle biopsies found to have variable muscle fiber sizes and even endomysial fibrosis may be markers of bent spine syndrome. In addition, disorganized internal architecture and little necrosis or regeneration is a marker of camptocormia.

Patients with camptocormia present with reduced strength and stooped posture when standing due to weakened paraspinous muscles (muscles parallel to the spine). Clinically, limb muscles show fatigue with repetitive movements. Paraspinous muscles undergo fat infiltration. Electromyography may be used as well in diagnosis. On average, the paraspinous muscles of affected individuals were found to be 75% myopathic, while limb muscles were 50% percent myopathic. Creatine kinase activity levels in skeletal muscle are a diagnostic indicator that can be identifiable through blood tests.