Like avascular necrosis, osteoporosis has been re-lated to steroids and to RT (Duthie and Katz, 1998; Tefft et al., 1976). Glucocorticosteroids inhibit new bone formation and calcium absorption and increase bone resorption and renal calcium excretion. Steroid-induced hypogonadism contributes to the problem in both men and women. More than 50% of patients tak-ing long-term steroids develop some degree of os-teoporosis (Goroll et al., 1995). The risk of devel-oping steroid-induced osteoporosis can be reduced by using a short-acting preparation at the lowest pos-sible dose in an alternate-day regimen, by maintain-ing physical activity, and by ensuring adequate daily intake of calcium and vitamin D. Treatments for os-teoporosis include 1. Therapies used to slow down bone involution and prevent contracture formation and postural deviations: weight-bearing exercises, upper and lower extremity muscle strengthening, balance training, back extension and chest expansion ex-ercises, pectoralis muscle stretching, posture correction, and proper lifting techniques 2. Cessation or tapering of glucocorticoid intake 3. Hormone replacement therapy for men and women who do not have contraindications 4. Thiazide therapy for hypercalcemia 5. Vitamin D and calcium supplementation when appropriate 6. Bisphosphonate therapy 7. Environmental modification: proper footwear, adjustment of medications that may contribute to falling; assistive devices 8. Education of patients regarding risk factors such as smoking Compression fractures may ensue with only minor trauma once sufficient structural integrity is lost. Pain may be managed with analgesic and anti-inflamma-tory medications and the use of spinal orthoses. Sur-gical fixation is sometimes necessary to attain stabil-ity. Early weight-bearing and limited immobilization should be encouraged to minimize continued bone loss. Contracture of Joints A limitation of passive joint range of motion, con-tracture commonly results from a restriction in con-nective tissue, tendons, ligaments, muscles, and joint elements. Contractures are most often related to spas-ticity, bed rest, localized heterotopic ossification, bleeding, infection, trauma, and edema. Prevention is achieved by minimizing the duration of bed rest and encouraging daily range of motion exercises. Heterotopic Ossification Heterotopic ossification is the formation of mature, lamellar bone in soft tissues. The variable incidence of heterotopic ossification has been reported in spinal cord injury patients (20% to 25%) and in head in-jury patients (10% to 20%) (An et al., 1987; Brooker et al., 1973; Evans, 1991; Garland, 1988; Ishikawa et al., 1982; Jensen et al., 1988; Stoikovic et al., 1955; Storey and Tegner, 1955; Stover et al., 1975). This condition has been observed in patients who require a prolonged ICU stay and is rarely seen in the cancer population. The chief symptoms of heterotopic ossi-fication are joint and muscle pain and compromised range of motion. A triple-phase bone scan is able to detect heterotopic ossification at an early stage. Ther-apies include bisphosphonates, nonsteroidal anti-inflammatory drugs, RT, and physical therapy. Pas-sive joint mobilization helps to maintain or increase joint mobility without promoting heterotopic ossification. Matured heterotopic ossification can be sur-gically excised. Shoulder Pain This problem often occurs in neurologically impaired populations. Shoulder pain may originate from rota-tor cuff tears, bicipital tendinitis, adhesive capsulitis, and subdeltoid bursitis. Other causes of shoulder pain in the hemiplegic population include excessive shoul-der capsule stretch secondary to paresis of shoulder musculature, sympathetically maintained pain (reflex-sympathetic-dystrophy, shoulder-hand syndrome), and thalamic syndrome. Management is diagnosis dependent. Immobilization syndrome may occur during recovery from operative or other treatments, be caused by medical complications, or result from the neurologic sequelae of cancer. It negatively impacts multiple body systems and often causes a decline in the pa-tient’s functional status. Immobilization can contrib-ute to intellectual, emotional, and behavioral distur-bances, decreased muscle strength and endurance, poor coordination, and contracture of joints. Car-diovascular and pulmonary deconditioning may pres-ent with orthostatic hypotension, deep vein thrombo-sis, decreased vital capacity, and impairment of the cough mechanism. Anorexia, constipation, electrolyte disturbances, and pressure ulcers are also manifes-tations of immobilization (Hoffman et al., 1998). The best management of this syndrome is through pre-vention. Physical therapy should begin early, empha-sizing progressive mobilization, starting with passive range of motion if necessary; progressing to assisted active range of motion; then to active range of mo-tion. When postural hypotension is pronounced or when patients have been or are expected to be bed bound for more than one week, tilt-table use should begin as soon as the patient is stable. This device is beneficial for cardiovascular and respiratory recon-ditioning and can also help prevent osteoporosis. Once the patient tolerates a 70-degree angle for 30 minutes, standing and ambulation should begin. Signs and symptoms of hypercalcemia, pressure ulcer, uri-nary tract infection, and pneumonia should be watched for vigilantly. Venous Thromboembolism Deep venous thrombosis (DVT) has a high incidence in stroke patients (30% to 50%) (Gibberd et al., 1976), in spinal cord injury patients (Merli et al., 1993; Weinmann and Salzman, 1994), after hip arthroplasty (Imperiale and Speroff, 1994), in pa-tients with cancer (Marik et al., 1997), and in im-mobilized patients (Giuntini et al., 1995). Elastic hosiery and sequential compression pumping of the calves should be continued until mobilization is un-derway. In spinal cord-injured and hemiplegic pa-tients, administration of subcutaneous low-molecu-lar-weight heparin is recommended. Exceptions are made for patients following intracranial surgery to avoid devastating hemorrhage. Patients with throm-bocytopenia, especially those with hematologic ma-lignancies and hemorrhagic tumors, require individ-ualized assessment, and their anticoagulation risks should be addressed with the primary oncology team.