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http://www.cs.odu.edu/~iat/papers/?autumn=term-paper-research-format-apa-web-sites-help term paper research format apa web sites help Abbreviations introduced in this chapter ach adls comt cr dbs dds gi icd mao nmda pd qol rbd rls trap updrs anticholinergics activities of daily living catechol-o-methyltransferase controlled-release deep brain stimulation dopamine dysregulation syndrome gastrointestinal impulse control disorder monoamine oxidase n-methyl-d-aspartate parkinson disease quality of life rapid eye movement sleep behavior disorder restless legs syndrome tremor, rigidity, akinesia/bradykinesia, postural/gait instability unified parkinson generic cialis work disease rating scale references 1. Nutt jg, wooten gf. Diagnosis and initial management of parkinson’s disease. N engl j med. 2005;353:1021–1027. 2. Lees aj, hardy j, revesz t. Parkinson’s disease. Lancet. 2009;373(9680):2055–2066. Review. Erratum in. Lancet. 2009. 374(9691):684. 3. Tanner cm, ross gw, jewell sa, et al. Occupation and risk of parkinsonism. A multicenter case-control study.

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http://cs.gmu.edu/~xzhou10/semester/thesis-paper-on-to-kill-a-mockingbird.html thesis paper on to kill a mockingbird Up to date. Waltham, ma. (accessed on october 25, 2014.) 27. Bates sm, greer ia, middeldorp s, et al. V e, thrombophilia, antithrombotic therapy, and pregnancy. Antithrombotic therapy and prevention o thrombosis, 9th ed. American college o chest physicians evidence-based clinical practice guidelines. Chest. 2012;141:E691s-d736s. 28. Linkins la, dans al, moores lk, bona r, davidson bl, schulman s, crowther m. American college o chest physicians. Reatment and prevention o heparin-induced thrombocytopenia. Antithrombotic therapy and prevention o thrombosis, american college o chest physicians evidence-based clinical practice guidelines. Chest. 2012 feb;141(2 suppl):E495s-e530s. 29. Marjoribanks j, farquhar c, roberts h, et al. Long term hormone therapy or perimenopausal and postmenopausal women. Cochrane database syst rev. 2012;7:Cd004143. Women’s issues in h ospit a l neur ology 30. Bond r, reraksem k, cu e r, et al. A systematic review o the associations between age and sex and the operative risks o carotid endarterectomy. Cerebrovasc dis. 2005;20:69-77. 31. Harden cl, pennell pb. Neuroendocrine considerations in the treatment o men and women with epilepsy. Lancet neurol.

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http://ccsa.edu.sv/study.php?online=honors-thesis-eku honors thesis eku Daily doses are limited to 10 mg because mao-b selectivity may be lost at higher doses increasing the risk of adverse effects and drug interactions. 27,28 rasagiline is less likely to cause insomnia because it is not metabolized to amphetamines. Side effects are primarily gi related. The labeling of rasagiline states that restriction of tyramine-containing foods is not ordinarily required at recommended dosages, but certain foods with extremely high levels of tyramine and exceeding recommend dosing of rasagiline may increase the risk of hypertensive crisis. 40 dyskinesias can be minimized by decreasing the levodopa dose when adding either of these agents. Because of risks of serotonin syndrome and hypertensive crisis, patients should avoid or use these medications cautiously with narcotic analgesics, antidepressants, and other serotonergic agents, or sympathomimetic amines (cold and weight loss products). 27,28 »» dopamine agonists dopamine agonists bind to postsynaptic dopamine receptors. They are useful as initial therapy, as suggested by the 2010 scottish intercollegiate guidelines. Their advantages include delay of levodopa therapy and smaller risk of developing motor fluctuations during the first 4 to 5 years of treatment. Eventually, they inadequately control the patient’s symptoms, and levodopa will need to be started. In advanced disease, they can be added to levodopa to minimize response fluctuations, decrease off time, improve wearing-off symptoms, allow a reduction in levodopa dose, and improve adls. 1,2,11,13,34,42 dopamine agonists include the ergot derivatives (bromocriptine) and the nonergot derivatives (rotigotine, pramipexole, ropinirole, and apomorphine). Generally, the nonergot agents are chosen first over bromocriptine due to a more favorable adverse effect profile and stronger evidence of efficacy. 43 if patients fail one dopamine agonist, another can be tried. Although not well established, it appears that bromocriptine 30 mg, ropinirole 15 mg, and pramipexole 4. 5 mg are equivalent, and this relationship can be a guide when switching agents. Rotigotine is available as a once-daily skin patch which minimizes pulsatile dopaminergic stimulation. 1,28,29,33,38 common side effects include nausea, vomiting, sedation (highest with apomorphine), pedal edema, orthostatic hypotension (highest with pramipexole) and psychiatric effects that are greater than with levodopa (nightmares, confusion, and hallucinations). Uncommon ergot side effects include painful reddish discoloration of the skin over the shins and pleuropulmonary, retroperitoneal, and cardiac fibrosis. 1,29,33,38 patients’ therapy may be complicated by the dopamine dysregulation syndrome (dds). This includes an addictive pattern of dopamine agonist use, complex stereotyped behavior known as punding, and impulse control disorders (icds) such as gambling or compulsive shopping. Reducing or eliminating the agonist usually resolves these problems. 44 dopamine agonists may cause excessive daytime sleepiness in 50% of pd patients. Sudden sleep attacks may occur and are potentially dangerous if occurring during certain activities such as driving. Modafinil and other agents to promote wakefulness may be used for daytime sleepiness, but use for sleep attacks remains controversial. 32,45 all dopamine agonists are metabolized by the liver except pramipexole, which is eliminated unchanged in the urine. Ropinirole is metabolized by cytochrome p450 and subject to drug– drug interactions with drugs that induce (eg, smoking) or inhibit (eg, ciprofloxacin, fluvoxamine, and mexiletine) cyp1a2. 29,33 apomorphine is used subcutaneously for acute off episodes in advanced pd when rapid rescue therapy is needed. It requires premedication with an antiemetic because it causes nausea and vomiting.

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http://www.cs.odu.edu/~iat/papers/?autumn=law-school-personal-statement-editing-service law school personal statement editing service O en presents as brown-sequard syndrome and progresses generic cialis work rapidly. It has a poor prognosis. Survival is o the order o 3–4 months. Given this, one may either do nothing, treat with steroids, or use radiation. ▲ figure 38-4 cystic lesion at the t11–t12 level within the spinal cord consistent with spinal cord hemangioblastoma in a patient with von hippel-lindau disease. 622 ch a pt er 38 part o neuro bromatosis type 1 syndrome. T ey can occur in two orms. Solitary—t ese are benign and cured by resection. Plexi orm—t ese a ect multiple roots and have dysmorphic nerve bundles incorporated within them. T ey have the capacity to become malignant and, in addition to surgery, may require radiation and chemical therapies. Extradural. Neoplastic seeding o the leptomeninges, depending on the type o tumor involved, is called carcinomatosis, lymphomatosis, or gliomatosis. T e most common tumors are breast cancer, lung cancer, melanoma, lymphoma, and acute leukemia. T e patient may present with a combination o radiculopathy, myelopathy, or cranial neuropathy. It is dif cult to diagnose as contrasted mri and csf cytology both have high alse-negative rates. Reatment is with intrathecal or systemic chemotherapy. Intrathecal chemotherapy may be administered with a lumbar puncture or with a subgaleal reservoir. Epidural mass. Epidural masses may be caused by vertebral or epidural metastases. T ere is o en bony vertebral pain, which is worse at night and with movement. What other epidural masses may x compress the cord?. Epidural hematomas caused iatrogenically or because o bleeding diatheses, or abscesses complicating lumbar puncture or hematologically seeded can also cause spinal cord compression. What are some o the indirect ways in x which myelopathy may occur in cancer patients?. Iatrogenic causes radiation spinal cord injury. T ese can be classi ed according to the time o presentation. Acute. T ese are due to leaky damaged vessels and are success ully treated with steroids. Early delayed. Occur weeks to months a er irradiation, also success ully treated with steroids (o en low doses). Late delayed. Radiation necrosis a er 4–24 months. Even when treated with steroids, the outcome is very poor. Chemotherapy-related toxic myelopathies. Most commonly due to intrathecal chemotherapy. Reatment is supportive. Paraneoplastic spinal disorders.

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