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achilles tendon disorders



foot pain, some forms GANGLION

Golfer's elbow/medial epicondylitis; see epicondylitis heel pain, some forms Housewife's knee; See prepatellar bursitis knee pain, some forms

Lateral epicondylitis/tennis elbow; see epicondylitis OLECRANON BURSITIS PLANTAR FASCIITIS ROTATOR CUFF SYNDROME

Tarsal tunnel syndrome; see foot pain


The word tendinitis implies inflammation of the tendon and was first described as an entity in 1763, although no doubt it was felt long before then. Tendons join muscles to bone and transmit the pulling force of the muscle. They are composed of spirals of collagen that are wrapped into bundles forming a thick cord that is both strong and able to stretch. Because of the property of viscoelasticity, a sudden rapid muscle contraction will find the tendon relatively stiff while slower contractions allow greater stretch. With repeated stretching the tendon becomes more flexible. While this applies to all ages, maximum flexibility does slowly decrease with increasing age. Longer tendons or those subject to significant friction are enveloped in a synovial sheath that has two layers that allow sliding to take place with little friction. Not all tendons have a sheath. The tendon gets its blood supply from both its muscle and the surrounding sheath if it has one. It attaches to the bone at an enthesis, and inflammation here (enthesitis) is described under ankylosing SPONDYLITIS and HEEL PAIN.

Inflammatory tendinitis can occur as part many conditions, including rheumatoid arthritis, anky-losing spondylitis, connective tissue diseases, psori-atic arthritis (see psoriasis and psoriatic arthritis), tuberculosis, gout, and giant cell tumors of the tendon. Most tendinitis, however, is due to mechanical strain and occurs following excessive repetitive movement or repetitive movement without adequate training. Tendinitis may also follow more acute injury, especially if activities are resumed before adequate healing has taken place. Tendon malalignment leading to the tendon having to transmit force at an angle to the line of its fibers commonly causes tendinitis. Impaired blood supply and fluoroquinolone antibiotics (see drug-induced rheumatic disease) are other causes. As a result of inflammation and scarring around the tendon, it can begin to stick or trigger. When this involves a tendon that curls a finger up, for example, the finger will be stuck in a curled position. often, with a little extra force, it will suddenly flick straight (trigger finger). This can also occur with stenosing tenosynovitis, in which the tendon sheath tightens around the tendon. This is sometimes familial. Cal-cific tendinitis has a dramatic onset, with pain made worse by movement. It can be caused by calcium apatite crystals or calcium pyrophosphate dihydrate deposition disease. Attacks are most common around the wrist, shoulder, and ankle.

Tendinitis is usually diagnosed by history and examination. If there is doubt or a possibility that there is a tear, then ultrasound is the best method to image tendons. It does, however, require an operator with experience in musculoskeletal ultrasound. MRI provides a good image of tendons and can also show up associated bone or joint problems. X rays will reveal calcific tendinitis and may show associated arthritic changes.

The type of immune response, damage, and repair mechanisms will differ among the different forms of tendinitis and between short-lived or long-lasting (chronic) problems. Treatment has to be directed to each individual's situation. ice and relative rest, for example using a wrist splint, are useful in settling the pain and swelling in most forms and in allowing healing to start. NSAIDs are effective but will seldom relieve pain to the extent that normal use is restored. This is a good thing since premature use is likely to lead to chronic tendinitis more often. if part of a generalized arthritis, better control of the disease as a whole may help. in these situations, however, injection of a small amount of corticosteroid often resolves the inflammation. These injections must be given into the sheath surrounding the tendon and not the tendon itself. Despite the severity of inflammation in cal-cific tendinitis, there is a concern that corticosteroid injections may slow resolution. Corticosteroid injections are also the first-line treatment for tendons that are triggering. Surgery may be necessary if these fail. Surgery to remove the debris from within a tendon can also lead to healing of chronic tendinitis (see also trigger finger, trochanteric bursitis; and wrist pain, some forms).

spinal stenosis A condition in which the spinal canal or nerve root canal does not provide adequate space for the spinal cord or nerve root to pass freely. Early reports of typical symptoms as well as operative findings date from the 1890s, well before the now more common disc protrusion was described. Spinal stenosis can affect the cervical spine (neck) or lumbar spine (lower back). The lumbar spine is affected much more often. patients are generally aged between 45 and 65 years, but younger and older patients may be affected. Men develop spinal stenosis more frequently than women, especially in the lumbar spine.


At least at the lower back level, the cross section of the spinal canal can be seen as a somewhat rounded triangle with equal sides, the base against the vertebral body and the apex pointing backward toward the spine. Spinal stenosis can occur at three sites at any given level. it can occur within the central spinal canal down which the spinal cord passes. it can occur in the lateral recesses that are the angles at each side of the base of the triangle. The nerve root angles into the lateral recess before entering the nerve root canal and leaving the spine. Finally, spinal stenosis can occur within the nerve root canal. Most of this discussion will refer to central canal stenosis, although the degenerative changes may affect all three sites.

Degenerative spondylosis is the most common cause both in the neck and back. This starts with wear and tear changes to the intervertebral disc. To a certain degree these are normal aging events. As the disc loses height a greater load is put onto the two smaller facet joints behind the spinal canal, the disc acting as a large joint in front of the canal. As a response to this increased load, the facet joint capsule thickens, and small bony outgrowths (osteophytes) grow out from the edges of the joints. Similarly, a rim of extra bone growth develops around the lip of the vertebral body, thus narrowing the canal space from all sides. in addition the powerful ligament that runs down the length of the spinal canal, the ligamentum flavum, thickens. This can thicken from a normal 2-5 mm in width to 5-10 mm, causing significant narrowing of the canal and compressing the cord. other degenerative changes may worsen the situation or, if severe, cause stenosis of their own accord. These include disc protrusion (see back pain), spondylolysis, and spondylolisthesis. Spondylolysis is a defect in the arch of bone from the vertebral body backward to the facet joints. Spondylolisthesis is the relative forward or backward movement of one vertebral body on another. in the presence of degenerative changes as described above spondy-lolisthesis can cause spinal stenosis with only 3-4 mm of movement. it seems likely that disturbance in the blood supply to the nerve root from compression of the very small arterioles surrounding the nerve plays a significant role in producing the symptoms of spinal stenosis.

people may have developmentally small spinal canals, and this is very common in people with achondroplastic dwarfism. Narrow canals have also been described in other families with no other bony problems. There is a range of canal width within the population, and those toward the narrow end of this range will be at greater risk of spinal stenosis.

There are a large number of rare causes of spinal stenosis. it may follow disc space infection, bony infection (osteomyelitis), tuberculosis of the spine, synovial cysts protruding into the canal and following trauma, or surgery. Excessive bone growth may also narrow the canal and cause compression. This can occur in paget's disease, ankylosing spondylitis or DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS, and acromegaly. gout and pseudogout (see calcium PYROPHOSPHATE CRYSTAL DEPOSITION DISEASE) have rarely been associated with spinal stenosis as has the development of benign fatty growths within the canal in people on long-term corticosteroids.

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