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However 10mg nolvadex amex, wide variation across MTFs on any given measure suggests that MTFs may not be providing care consistently discount nolvadex 20mg mastercard, which could include overtreatment in some cases and undertreatment in others order nolvadex 10 mg mastercard. DISTRIBUTIONS OF MTFs ON LOW BACK PAIN MEASURES Presented here is a series of figures (Figures 3 purchase nolvadex 20mg amex. The first bar on the left of each graph is the overall average baseline performance for all nine MTFs generic 20 mg nolvadex mastercard, and the remaining bars show the values for each of the nine MTFs. To protect the confidentiality of individual MTFs, the results are reported anonymously (Cs are control MTFs, and sites are demonstration sites). Baseline Performance of the Study Sites 31 We tested the statistical significance of the differences of MTF values by comparing each MTF’s average value for a measure to the average value for the remaining eight MTFs. When the performance of an MTF differs significantly from the average of the other MTFs, the MTF’s label in the legend is followed by asterisks (* for p < 0. As discussed in Chapter Two, both the clinical significance of observed differences among MTFs and the statistical significance of these differences should be considered when interpreting these results. The referral rates for physical therapy or manipulation services were significantly lower than average for three MTFs and were significantly higher for three other MTFs (Figure 3. The MTFs with the lowest and highest rates of primary care visits differed by almost 80 percent (Figure 3. One MTF had an average rate that was 100 percent higher than the mean and an- other had a rate that was 50 percent lower. An overall aver- age of 50 percent of acute low back pain episodes treated by the nine MTFs had prescriptions for muscle relaxants. This rate compares with a rate of 35 percent of civilian patients being prescribed muscle relaxants found in a Seattle study (Cherkin et al. It also con- trasts strongly to the guideline recommendation against any use of RANDMR1758-3. Rates of muscle relaxant use were significantly lower than the overall average for only two MTFs, while rates were significantly higher for five MTFs (Figure 3. Two MTFs had significantly lower rates of narcotics use, and four had significantly higher rates (Figure 3. Finally, rates of prescription of high-cost NSAIDs were low, on average, but varied significantly across MTFs (Figure 3. Two MTFs had rates much higher than the average, and three MTF had rates that were only one- third lower than average. First, there is substantial variation among the MTFs in the rates of use for physical therapy/manipulation ser- vices, primary care visits, and specialty referrals. Second, there are consistently high percentages of patients prescribed muscle relax- ants or narcotic pain relievers, neither of which are recommended by the guideline because scientific evidence does not support their use for acute low back pain. Third, providers at a few MTFs appear to be using high-cost NSAIDs for their patients at high rates compared with the other MTFs, although the overall rate of use is low (an aver- age of 4 percent of patients used high-cost NSAIDs across all MTFs). For example, a prior- ity clearly could be placed on reducing use of muscle relaxants by working with providers to change their prescribing methods. This is a particularly good example because there is such strong scientific evi- dence against using muscle relaxants, and providers are prescribing them for one-half of the patients in the study sample. The wide variation across MTFs for the three service use indicators raises the question, What is the desired rate of use, for which there is no real "gold standard? For example, an MTF may have a baseline rate of physical therapy referrals that is 50 percent higher than the mean but remains in the realm of clinical appropriateness. Conversely, the use rate for muscle relaxants for the MTF with the lowest rate may still be too high, which would also be cause for con- cern. Chapter Four INFRASTRUCTURE FOR GUIDELINE IMPLEMENTATION The implementation teams at the demonstration MTFs were re- sponsible for working with MTF primary care clinics to introduce practices recommended by the guideline for low back pain manage- ment, but they were not expected to carry out these changes alone. MEDCOM and RAND provided instructions to the MTFs regarding the organization of the MTF implementation teams and activities, encompassing both support by the MTF command and a clear focus of leadership and membership for the implementation teams. MED- COM also made a commitment to provide corporate support in the form of policy guidance regarding recommended practices, tools and materials for MTF use in implementing those practices, and monitoring of progress in achieving new practices. In this chapter, we report our findings regarding the infrastructure established for the low back pain guideline demonstration. Then we de- scribe the MTF support structure, including support by the MTF command team and roles of the guideline champions, facilitators, and implementation teams. MEDCOM SUPPORT The corporate responsibility for operating the AMEDD program for evidence-based practice guidelines was assigned to the MEDCOM Quality Management Directorate.

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The pool temperature should be about 85 degrees; this may feel cold to some people order 10 mg nolvadex mastercard, but warmer tempera- tures should be avoided because they produce fatigue buy generic nolvadex 20 mg line. Colder tem- peratures can actually cause spasticity buy 20mg nolvadex amex, thus the temperature of the pool is quite important 20 mg nolvadex fast delivery. Many people with MS have a limited range of movement in at least some joints and muscles buy nolvadex 20mg, and the key to managing spasticity 35 PART II • Managing MS Symptoms is to expand the number and kind of movements that can be per- formed. The key to managing spasticity is to expand the number and kind of movements that can be performed. Spasticity also may be reduced by the use of relaxation tech- niques that involve a combination of progressive tensing and relax- ing of individual muscles, accompanied by deep breathing tech- niques and imagery. MECHANICAL AIDS Specific devices sometimes are made for certain individuals to counteract spasticity and prevent what are termed contractures, in which the range of movement possible for a given joint becomes restricted as the result of spasticity. For example, a "toe spreader" or "finger spreader" is used to relax tightness in the feet and hands and to aid in mobility. Braces for the wrist, foot, and hand are used to maintain a natural position and to prevent limitations on move- ment and the development of deformities. MEDICATIONS Spasticity often is managed most effectively by medications (see table). Baclofen acts on the nerves that control the spastic muscles 36 CHAPTER 4 • Spasticity at their site of origin in the spinal cord. It is the most common anti- spasticity medication used in MS, and most people respond well to it. The dose must be carefully determined for each individual; too little will be ineffective, whereas too much produces fatigue and a feeling of weakness because it interferes with the proper degree of stiffness needed for balance and erect posture. The correct dose usually is determined by starting at a low level and slowly increas- ing the dose until a maximal beneficial effect is obtained. The most common mistake when taking baclofen is to give up on it too soon, so that the dose never reaches the level necessary to attain proper relaxation. That dose may be as low as one half of a pill (5 mg) per day, but some people may need to take as much as 40 mg four times a day. Baclofen is only available as a generic and may be the least expensive medical treatment. Medications for the Management of Spasticity Medication Notes Baclofen May produce weakness at higher dose Tizanidine (Zanaflex® O ften combined with baclofen; may produce drowsiness Sodium dantrolene May produce weakness (Dantrium®) Diazepam (Valium® H ighly sedating; most often used at night; may become addictive Clonazepam (Klonopin®) Sedating; most often used at night Cyproheptadine HCl Sedating; used primarily as an (Periactin® "add on" medication Cyclobenzaprine HCl Used for back spasms; most (Flexeril®) often combined with other medications (continued on next page) 37 PART II • Managing MS Symptoms Medications for the Management of Spasticity (continued) Medication Notes Gabapentin (Neurontin® May ease spasms that are diffi- cult to manage L-dopa (Sinemet®) Especially useful for nighttime spasms Selegiline (Eldepryl®) Especially useful for nighttime spasms Carbamazepine (Tegretol®) Used for flexor spasms of the arm or leg Cortisone Effective for paroxysmal spasms; should only be used on short- term basis Tizanidine (Zanaflex®), a newer antispasticity medication, acts on a different area of the spinal cord than baclofen. It appears to be effective in decreasing stiffness and muscle spasm, with less effect on strength than many other drugs. It must be used carefully and slowly because sleepiness inevitably results if the dose is increased too rapidly. This appears to have something to do with the lack of outside stimulation to the nervous system, making it more sensitive to spasm. Another medication that sometimes is used for spasticity is sodium dantrolene (Dantrium®), which acts directly on muscles. Its calming effect also helps to induce sleep, but its strong sedative effect limits its use during the daytime. Diazepam must be pre- scribed with caution because it may become addictive if it is used too frequently. It produces significant relaxation, and thus may be used as an anti- spasticity medication. When using diazepam or clonazepam, both the doctor and the person with MS must pay attention to the potential for chemical dependency. However, if the dose must be continu- ally increased and the person is using the medication not for spas- ticity but as a crutch to escape the realities of the world, it should no longer be used. Cyproheptadine (Periactin®) is an antihistamine that has anti- spasticity properties and may be a good add-on medication at cer- tain times. Its sedating effect limits its use, but doses of 4 mg taken when needed may be helpful. A drug that is commonly used for spasms in the muscles of the back is cyclobenzaprine HCl (Flexeril®). It usually works best in combination with one of the other antispasticity medications. Gabapentin (Neurontin®) is a newer medication that has been approved for use in seizures. This medication also has antispastici- ty properties, and when it is taken in doses of over 1 gm per day often eases problematic spasms.

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By going through some illustrative examples we can get a sense of why the category of disease has ramified to include so much 20mg nolvadex otc, but also of how the less central diseases deviate from the prototype buy 20 mg nolvadex free shipping. Cancer Cancer is a collection of very different diseases often casually considered as one because of the common feature of cell growth escaping from normal control purchase nolvadex 20mg on-line. There might have been something wrong with the victim that predisposed to cancer purchase nolvadex 20 mg fast delivery, even if she felt well nolvadex 20mg. There is a whole grab bag of proven and alleged causal factors, not a single outstanding discrete cause. It may be that single primary causes (like asbestos for mesothelioma) will be found for more and more varieties of cancer, but even when we know of viruses causing human malignancies, such as Epstein-Barr virus causing Burkitt’s lymphoma, the relationship of the etiologic agent to the disease is far from one to one. So many other confounding factors are present that the virus is not understood in simple fashion as "the" cause. The causal factors do not necessarily come from outside the person, since there are inborn cancers, inherited syndromes causing cancers, idiopathic (etiologi- cally obscure) cancers, intrinsic resistance or susceptibility factors and behaviors increasing known environmental risks. Regarding the remaining cardinal "disease" features listed under the prototype, cancer is in the main similar. The central cognitive model is still Disease Is War with the useful modification that the victim is being undermined and "eaten from within" by an enemy. Accordingly, the disease "infiltrates," may be "insidious" and is "the body turning against itself. Finally, cancer is most common in the elderly, and thus seems more like a "real" disease and not a normal accompaniment of aging when it occurs in younger victims. Vascular Accidents In considering vascular accidents such as heart attacks, strokes and emboli (dislodged clots which migrate) it is evident that these conditions diverge differently from the prototype than does cancer. Even with a striking sudden initial episode there is the presumption (after the shock wears off), of prior "latent" or "occult" disease such as atherosclerosis, which has become manifest in the attack. The causes do not clearly originate outside the person, from the standpoint of medical science, but in habits, environment and inherited factors together. Thus the disease, upon reflection, is not entirely alien to the "self," broadly considered. Here and with many other diseases there is often a divergence in the HEALTH AND DISEASE 61 view initially taken by the caregiver and the victim, which may only be partially resolved later as they come to understand one another better. The victim has an interest in distancing her or himself as far as possible from the disease. This means that the victim has an interest in construing a part of the body from which the disease came (also in the case of cancer) as radically separated from the self. This sort of thinking is ready to hand because in everyday experience so many perspectives on and parts of our own bodies are unavailable and hidden from our own consciousness. Yet, when health is running smoothly we like to take credit for it as part of ourselves and self-worth. The patient, on the other hand, is understandably in conflict because she needs a strong self to "fight" the illness and incorporation of the illness into herself is contrary to that need. Frequently, our narratives of illness or aging have to do with attitudes we take toward infirmities including owning or disowning them. The causes of vascular disease and accidents are mostly physical, but personality factors and environmental stresses may yield "psychosomatic" effects on the circulatory system. The causes primarily affect the body but secondary psychosocial effects such as depression are often more important than with an illness like pneumonia. The victim is aware of being ill, but only after a presumed "silent" or latent process has become manifest. Because of the divergence between patients, who focus on the acute, disruptive and difficult to assimilate aspects of the disease and professionals who see these as outcomes of a long underlying process, the cognitive models and other portrayals of vascular disease are not uniform. The victim, and to a lesser extent the physicians, use language which maps injury and often assault on vascular disease. Delicate physiological processes, often "balances," are upset and the body attempts "compensation" for the damage which was originally caused by various excesses and deficiencies. The upshot is that cardiovascular disease in its diverse aspects can be thought of in terms of attack, injury, imbalance or mechanical breakdown ("heart failure").

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There are several hypotheses concerning the mechanisms involved in the pathophysi- ology of central pain buy nolvadex 20 mg without a prescription. Head and Holmes (1911) proposed a disinhibition of the STT-thalamocortical system nolvadex 10mg line, triggered by lesions of the DCN-medial lemniscus system discount 20 mg nolvadex free shipping. Foerster’s hypothesis (1936) was similar: he thought that epicritic sensitiv- ity (touch generic 20 mg nolvadex with mastercard, pressure order 20mg nolvadex with visa, vibration) normally exerts control over protopathic sensitivity (pain and temperature). According to Foerster’s hypothesis, central pain can only occur when there is a loss of epicritic sensitivity, e. More recently, indications were repeatedly found that the STT system is affected in the majority of patients with central pain (Boivie et al. Central pain patients have abnormal temperature and pain sensibility, but they may have normal threshold to joint movements, vi- bration, and touch (Boivie et al. Low brainstem infarcts (Wallenberg syndrome) and cordotomies, in which the STT but not the medial lemniscus is interrupted, may cause central pain (Boivie et al. This kind of lesion leave the more medially and inferiorly terminating paleo-STT projections intact (Boivie 1999). Another hypothesis focuses on the role of the reticular thalamic nucleus, and the medial and intralaminar zones receiving STT fibers. The reticular nucleus is the only thalamic nucleus built by GABAergic, inhibitory projection neurons that do not give rise to thalamocortical fibers but heavily innervate the remaining thalamic nuclei (Gonzalo-Ruiz and Lieberman 1995; Guillery et al. According to this hypothesis, the lesion removes the suppressing activity exerted by the reticular thalamic nucleus on intralaminar and medial thalamic nuclei, thereby releasing abnormal activity in this region, which in turn leads to pain and hypersensitivity (Cesaro et al. Recently Craig (1998, 2003d) put forward a new hypothesis about the mecha- nisms of central pain. Central pain is due to the disruption of thermosensory integra- 66 Neuropathic Pain tion and the loss of cold inhibition of burning pain. This disruption is caused by a lesion along the STT to the nuclei VPI, VMpo, and MDvc. These projections tonically inhibit nociceptive thalamocortical neurons, which by the lesion increase their firing and produce pain. The pathway is activated by cold receptors in the periphery, which in turn activate cold-specific and polymodal lamina I cells in the DH. According to Boivie (1999), this hypothesis might be applicable in some patients, but not in others, because of the location of the lesions and the character of the pain (roughly 40%–60% of all central pain has a burning character). Chronic pain or NP can result from damage of the nervous system at different levels of pain processing: peripheral nerve, SG, dorsal root, CNS. Chronic syndromes mostly show positive symptoms such as pain, dysesthesia, and paresthesia, often in combination with negative symptoms such as sensory deficits. Unfortunately, pharmacotherapy of NP is limited, perhaps because the etiology, the mechanisms, and the symptoms of NP may differ considerably be- tween patients. In patients with PHN pain, mainly peripheral mechanisms are discussed as being involved, but central changes might also be involved. Periph- eral neuropathic pain is a spontaneous pain (stimulus-independent pain) or a hy- persensitivity pain caused by a stimulus following damage of sensory neurons (stimulus-evoked pain). Inflammation in the DG can sensitize neurons to respond to normal innocuous thermal or mechanical stimuli and loss of DG perikarya can induce changes in surrounding surviving neurons. Thus, loss of sensory den- drites in the epidermis of patients suffering from PHN was positively correlated with both sensory deficits and with pain (Baron and Saguer 1993; Koltzenburg et al. Changes caused by alterations of peripheral input, followed by altered spinal processing can be forwarded to the cortex via thalamic nuclei (Coderre et al. Neurons in the somatosensory thalamus of patients with NP showed various electrophysiological abnormalities: responses to stimuli of body regions not normally driving those cells, high spontaneous firing rates, and abnormal bursting activities. Thus, besides peripheral and spinal changes there is massive cortical plasticity contributing to the development of pathological pain. In NP, a change related to chronicity and amount of pain was reported (Flor 2003). Moreover, using 1H-MRS chemical changes were noted in the dorsolateral prefrontal cortex in chronic back pain for N-acetyl aspartate and glucose, which could be related to measures of pain and anxiety (Grachev et al.

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