By W. Marius. South Dakota School of Mines and Technology.
Kovar et al20 studied two four-week exercise programs: individual weight bearing exercises and supervised group therapy consisting of non-weight bearing exercises order 500 mg hydrea with amex medicine zocor. This study concerned patients with knee OA for a mean duration of > 10 years proven hydrea 500mg treatment gastritis, while participants were recruited from the community and the clinic. The intervention concerned an eight week supervised group therapy that mainly consisted of “fitness walking”. Other studies concerned patients with knee OA according to criteria of the American College of Rheumatology who were recruited from both the community and the clinic,15 and patients with knee OA (not specified) who were recruited in the clinic11 and included exercise interventions consisting of a 12 week walking programme15 or an 8 week strength training programme monitored on a dynamometer11. Thus, the evidence indicates a small to moderate beneficial effect of exercise therapy on pain in knee OA. This effect was found in participants with minimal-moderate OA who recruited from both community and clinic and were being treated with various types of exercise therapy for at least eight weeks. Self reported disability Self reported disability was measured in six trials. In one trial,11 data presentation was 187 Evidence-based Sports Medicine insufficient to calculate the effect of exercise on disability. In two trials with sufficient power,2,10 small effects on disability were observed. Among the three trials with low power,15,19,20 a large effect in two of the three trials19,20 was observed. It can be concluded that there is evidence for a small beneficial effect of exercise on self reported disability. This effect was found in participants with minimal to moderate OA who were recruited from both community and the clinic and were being treated with various types of exercise therapy. In these trials, five different assessments were used. In two trials11,17 data presentation was insufficient to calculate the effect size. In three trials with sufficient power2,10,23 a small beneficial effect of exercise therapy on walking performance was observed. Petrella and Bartha14 observed increased walking at self pace and self paced stepping (two measures of clinical relevance) following their exercise intervention. In conclusion, the evidence indicates a small beneficial effect of exercise therapy on walking performance while Petrella and Bartha14 showed significant effect on both self selected speed of walking and stepping; both clinically relevant functional outcomes as recommended by OMERACT. Discussion Recent guidelines have advocated inclusion of exercise in treatment of osteoarthritis of the knee6. However, past reports of exercise as an etiologic factor in osteoarthritis of weight bearing joints3–5 may have reduced implementation among physicians. Further, lack of standard protocols, outcome measures and maintenance strategies may have also contributed to poor exercise implementation. A large, randomised, multicentre study by Ettinger et al10 showed that older patients who engage in either resistance or aerobic exercise achieved better pain control and functional outcomes at 18 months compared to patients who only attended an educational programme. However, patients in that study continued to take various arthritis medications while in the study, and there was no attempt to control for the class of medication. This may make decisions regarding inclusion of exercise difficult for practitioners. We recently reported the effect of a brief home-based, progressive resistance exercise programme for patients with unilateral osteoarthritis of the knee. Compliance with the program at two months was over 96%, no adverse events were reported and pain and physical functioning measured using a self paced walking activity significantly increased from baseline. Despite these positive findings, no dose- response relationship between aerobic or resistance exercise and osteoarthritis has been established. In addition, issues of long-term adherence and efficacy for exercise in the treatment of osteoarthritis are still unresolved. One other application of exercise therapy is the interaction with intra-articular hyaluronate. Petrella et al28 have recently completed a randomised trial of home-based exercise therapy in addition to three intra-articular hyaluronate (10mg/ml) injections and found this combination improved “activity-related” pain more than when exercise was combined with NSAID. These and other future well designed studies combining exercise with neutriceutical products including glucosamine sulfate will further our ability to ensure comprehensive treatment of patients with osteoarthritis of the knee. Key findings Seventeen randomised controlled trials of the effectiveness of exercise therapy in OA of the knee were assessed. It can be concluded, 189 Evidence-based Sports Medicine that exercise is effective in patients with OA of the knee.
It can directly scavenge hydroxyl radicals generic hydrea 500 mg with visa medicine 751, oxyheme oxidants formed between the reaction of hemoglobin and peroxy radicals cheap hydrea 500 mg online medicine remix, and peroxyl radicals them- selves. Having acted as a scavenger, uric acid produces a range of oxidation products that are subsequently excreted. Melatonin, which is a secretory product of the pineal gland, is a neurohor- mone that functions in regulation of our circadian rhythm, light–dark signal transduction, and sleep induction. In addition to these receptor-mediated func- tions, it functions as a nonenzymatic free radical scavenger that donates an elec- tron (as hydrogen) to “neutralize” free radicals. It also can react with ROS and RNOS to form addition products, thereby undergoing suicidal transformations. Its effectiveness is related to both its lack of pro-oxidant activity and its joint hydrophilic/hydrophobic nature that allows it to pass through membranes and the blood-brain barrier. O HN N OH O N N H H Uric acid H O CH3O CH2 CH2 CH3 N H Melatonin Fig 24. Uric acid and melatonin both act to successively neu- tralize several molecules of ROS. The pathogenesis of this Fe2+ 2 disease is not well established and may be multifactorial (Fig. The major clinical disturbances in Parkinson’s disease are a result of dopamine •OH O – 2 depletion in the neostriatum, resulting from degeneration of dopaminergic neurons NO whose cell bodies reside in the substantia nigra pars compacta. The decrease in dopamine production is the result of severe degeneration of these nigrostriatal neu- RNOS rons. Although the agent that initiates the disease is unknown, a variety of studies 3 support a role for free radicals in Parkinson’s disease. Within these neurons, Lipid peroxidation dopamine turnover is increased, dopamine levels are lower, glutathione is Protein oxidation DNA strand breaks decreased, and lipofuscin (Lewy bodies) is increased. Iron levels are higher, and fer- ritin, the storage form of iron, is lower. Furthermore, the disease is mimicked by the 4 Lipofuscin compound 1-methyl-4-phenylpyridinium (MPP ), an inhibitor of NADH dehydro- Neuronal genase that increases superoxide production in these neurons. Even so, it is not degeneration known whether oxidative stress makes a primary or secondary contribution to the disease process. Drug therapy is based on the severity of the disease. In the early phases of the Reduced dopamine release disease, a monoamine oxidase B-inhibitor is used that inhibits dopamine degrada- tion and decreases hydrogen peroxide formation. A model for the role of ROS and patients are treated with levodopa (L-dopa), a precursor of dopamine. RNOS in neuronal degradation in Parkinson’s disease. Dopamine levels are reduced by Cora Nari experienced angina caused by severe ischemia in the ventric- monoamine oxidase, which generates H2O2. Superoxide also can be produced by mito- the site of atherosclerotic plaques within the lumen of the coronary arter- chondria, which SOD will convert to H2O2. When TPA was infused to dissolve the clots, the ischemic area of her heart was reaction to proceed, generating hydroxyl radi- reperfused with oxygenated blood, resulting in ischemic–reperfusion injury. NO, produced by inducible nitric oxide case, the reperfusion injury resulted in ventricular fibrillation. The RNOS and hydroxyl radical decreased O2 supply results in decreased ATP generation from mitochondrial oxida- lead to radical chain reactions that result in tive phosphorylation and inhibition of cardiac muscle contraction. As a conse- lipid peroxidation, protein oxidation, the for- quence, cytosolic AMP concentration increases, activating anaerobic glycolysis and mation of lipofuscin, and neuronal degenera- lactic acid production. If ATP levels are inadequate to maintain Na ,K -ATPase tion. The end result is a reduced production activity, intracellular Na increases, resulting in cellular swelling, a further increase and release of dopamine, which leads to the in H concentration, and increases of cytosolic and subsequently mitochondrial clinical symptoms observed. The decrease in ATP and increase in Ca may open the mitochondrial permeability transition pore, resulting in permanent inhibition of oxidative phos- phorylation. Damage to lipid membranes is further enhanced by Ca2 activation of phospholipases. Reperfusion with O2 allows recovery of oxidative phosphorylation, provided that the mitochondrial membrane has maintained some integrity and the mitochondrial transition pore can close.
The long history of physical therapy has been predominated by different theories of development and specific protocols to impact childhood devel- opment discount hydrea 500 mg fast delivery symptoms bone cancer. In this theory the spinal cord-mediated activities order 500 mg hydrea amex symptoms ptsd, such as single synapse reflexes and spasticity, have to be corrected first be- fore the more primitive higher reflexes can be addressed. These primitive reflexes then have to be corrected before high-functioning cortical motor 5. Therapy, Education, and Other Treatment Modalities 153 activities, such as walking, can develop properly. This hierarchical theory of neurologic development has some base in animal studies. For example, the need for the eye to function properly before the optical cortex will organize and function appropriately is well documented. The scope of this text, however, makes it impossible to give a full discription of these techniques. In the 1990s, the theory of neurologic development was slowly changing to a more complex, circular theory in which subsystems are recognized to interact. In this the- ory, the psychologic state and behavior of children are also recognized as be- ing important in their motor function. Complex interactions exist between lower reflexes and cortical motor movement patterns, in which the inter- actions and impacts are both from the higher function to the lower function and vice versa. However, this change in approach is not universally adapted, because neurologic pediatric physical therapy is a small subspecialty of the much larger physical therapy discipline. In gen- eral, physical therapists tend to have clinical aptitudes that are similar to those of orthopaedic surgeons. Clinicians with a treatment approach like to identify a specific problem, then apply a cure to make the problem go away. This approach was feasible in the early therapy protocols based on the hier- archical development theory; however, it often frustrated the child, the family, and the therapist. Developing a concept where the child, family, physician, and therapist are one team whose goal is to make the child as in- dependent as he or she can be when growing up is a much more functional approach. With this approach, an experienced therapist is the ideal head coach of the team, because this is the individual who knows the child best from a medical perspective and has the best relationship with the child, family, educators, and physicians. Unfortunately, because of frequent changes in therapists, this role of head coach often falls to the family. For some fam- ilies, this works well, but for others, it does not. The therapist who takes on the role of coach of a child’s motor impair- ment management team has to develop a good relationship with the family and child. In general, this relationship does not work well if the parent or child does not like the therapist. Also, the therapist has to have some under- standing of behavior management techniques to get the most cooperation from a child. Being aware of medical and other family issues is also important. The physical therapist should understand how to access social services and medical help in the community that may be needed by the family. One of the problems of this expanded role of pediatric therapists is that many therapists do not believe they have the training needed to take on this role. Most phys- ical therapy training programs are at the master’s degree level; however, the amount of training in pediatrics is minimal in many programs where there is a much greater allure to sports medicine and other adult rehabilitation di- rections. This experience mirrors what happens in orthopaedic training. Currently, there are a few well-developed specialty training programs for pe- diatric therapists, and none as well organized as the fellowship programs in pediatric orthopaedics. The trend to standardize this pediatric training is moving ahead and should train therapists who are much better equipped to take on the role in which they are currently expected to function.