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TABLE 9.3 Phlebectomy Supplies Skin marking pen Iodine prepping solution Disposable face mask, sterile gloves Local anesthetic, syringes, needles Ambulatory phlebectomy hooks: Muller, Oesch, Ramelet, Varady Clamps, sterile 4 4 gauze pads NoCor 18-gauge needle, scalpel No. 11 Mosquito forceps (one dozen) Hydrogen peroxide for postoperative washing of the leg Absorbent dressings Inelastic compression wrap Elastic graduated compression stockings
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PRINEAS JW, MCLEOD JG: Chronic relapsing polyneuritis. J Neurol Sci 27:427, 1976. RAFF MC, SANGALANG V, ASBURY AK: Ischemic mononeuropathy multiplex associated with diabetes mellitus. Arch Neurol 18:487, 1968. RECHTHAND E, CORNBLATH DR, STERN BJ, MEYERHOFF JO: Chronic demyelinating polyneuropathy in systemic lupus erythematosus. Neurology 34:1375, 1984. REFSUM S: Heredopathia atactica polyneuritiformis: A familial syndrome not hitherto described. Acta Psychiatr Scand Suppl 38:1, 1946. ROBSON JS: Uraemic neuropathy, in Robertson RF (ed): Some Aspects of Neurology. Edinburgh, Royal College of Physicians, 1968, pp 74 84. ROGERS LR, BORKOWSKI JW, ALBERS KH, et al: Obturator mononeuropathy caused by pelvic cancer: Six cases. Neurology 43:1489, 1993. ROMERO CE, JACOBS BJ, ROPPER AH: Clinical characteristics of a mild sensory-fasciculatory syndrome. Neurology 62(suppl 5):A519, 2004. ROPPER AH: Unusual clinical variants and signs in Guillain-Barre syn drome. Arch Neurol 43:1150, 1986. ROPPER AH: Severe acute Guillain-Barre syndrome. Neurology 36:429, ` 1986. ROPPER AH: The Guillain-Barre syndrome. N Engl J Med 326:1130, 1992. ROPPER AH: Accelerated neuropathy of renal failure. Arch Neurol 50:536, 1993. ROPPER AH: Further regional variants of acute immune polyneuropathy. Arch Neurol 51:671, 1994. ROPPER AH: Chronic demyelinating polyneuropathy: Improvement after sepsis. Neurology 46:848, 1996. ROPPER AH, GORSON KC: Neuropathies associated with paraproteinemias. N Engl J Med 338:1601, 1998. ROPPER AH, KEHNE SM: Guillain-Barre syndrome: Management of res piratory failure. Neurology 35:1662, 1985. ROPPER AH, MARMAROU A: Mechanism of pseudotumor in GuillainBarre syndrome. Arch Neurol 41:259, 1984. ROPPER AH, WIJDICK EFM, TRUAX BT: Guillain-Barre Syndrome. Phil adelphia, Davis, 1991. ROWLAND LP, DEFENDINI R, SHEMAN W, et al: Macroglobulinemia with peripheral neuropathy simulating motor neuron diseases. Ann Neurol 11: 532, 1982. RUKAVINA JG, BLOCK WD, JACKSON CE, et al: Primary systemic amyloidosis: A review and an experimental genetic and clinical study of 29 cases with particular emphasis on the familial form. Medicine 35:239, 1956. SABIN TD: Temperature-linked sensory loss: A unique pattern in leprosy. Arch Neurol 20:257, 1969. SAID G: Perhexiline neuropathy: A clinicopathologic study. Ann Neurol 3: 259, 1978. SAID G: Vasculitic neuropathy, in Hartung HP (ed), Peripheral Neuropathies: Balliere s Clinical Neurology, part I, vol 4. London, Balliere Tin dall, 1995, pp 489 503. SAID G, ELGRABLY F, LACROIX C, et al: Painful proximal diabetic neuropathy: In ammatory nerve lesions and spontaneous favorable outcome. Ann Neurol 41:762, 1997. SAID G, LACROIX C, LOZERAM P, et al: In ammatory vasculopathy in multifocal diabetic neuropathy. Brain 126:376, 2003. SAID G, LACROIX C, PLANTO-BORDENEVUE U, et al: Nerve granulomas and vasculitis in sarcoid peripheral neuropathy. Brain 125:264, 2002. SAID G, SLAMA G, SELVA J: Progressive centripetal degeneration of axons in small ber type diabetic polyneuropathy: A clinical and pathological study. Brain 106:791, 1983. SAMANTA A, BURDEN AC: Painful diabetic neuropathy. Lancet 1:348, 1985. SANDRONI P, VERNINO S, KLEIN CM, et al: Idiopathic autonomic neuropathy. Comparison of cases seropositive and seronegative for ganglionic acetylcholine receptor antibody. Arch Neurol 61:44, 2004. SARAIVA MJM, COSTA PP, GOODMAN DS: Genetic expression of a transthyretin mutation in typical and late-onset Portuguese families with familial amyloidotic polyneuropathy. Neurology 36:1413, 1986.
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Determining the oxidation state of a specific carbon atom is simple. Just count the number of carbon and hydrogen atoms that the carbon atom in question is connected to. Carbon carbon double bonds count only once. A more reduced carbon has a higher number, and a more oxidized carbon has a lower number. Carbon atoms can be in five different oxidation states.1 Being in a different oxidation state means that some source of oxidizing or reducing agent must be used to convert carbon in one oxidation state to carbon in another oxidation state. In terms of the table following, this means that to move up in the table (to a more reduced form of carbon) requires a reducing agent such as NADH. Moving down the table requires an oxidizing agent such as NAD or oxygen. Moving between successive oxidation states represents a two-electron oxidation or reduction. Conversion of carbon within a given redox state does not require an oxidizing or reducing agent.
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destruction that leads to disease. In contrast, familial cases of prion disease are thought to be the result of one of several gene aberrations residing in the region that codes for PrPc. Of some interest is the nding by Zanusso and colleagues of the infectious prion protein in the nasal mucosa of all nine patients studied with the sporadic disease. This suggests a route for entry into the nervous system of the aberrant prion and also a potential diagnostic test. Clinical Features Transmissible SSE is in most cases a disease of late middle age, although it can occur in young adults. The sexes are affected equally. In the large series of pathologically veri ed cases reported by Brown and coworkers, prodromal symptoms consisting of fatigue, depression, weight loss, and disorders of sleep and appetite lasting for several weeks were observed in about one-third of the patients. The early stages of the disease are characterized by a great variety of clinical manifestations, but the most frequent are changes in behavior, emotional response, and intellectual function, often followed by ataxia and abnormalities of vision, such as distortions of the shape and alignment of objects or actual impairment of visual acuity. Typically, the early phase of the disease is dominated by symptoms of confusion, with hallucinations, delusions, and agitation. In other instances, cerebellar ataxia (Brownell-Oppenheimer variant) or visual disturbances (Heidenhain variant) precede the mental changes and may be the most prominent features for several months. Headache, vertigo, and sensory symptoms are complaints in some patients but become quickly obscured by dementia and muteness. As a rule, the disease progresses rapidly, so that obvious deterioration is seen from week to week and even day to day. Sooner or later, in almost all cases, myoclonic contractions of various muscle groups appear, perhaps unilaterally at rst but later becoming generalized. Or, infrequently, the myoclonus may not appear for weeks or even months after the initial mental changes. The myoclonus is associated with a striking startle response, mainly to a loud noise. In a few patients, a startle response, which is elicitable for a brief period of time, is the only manifestation of myoclonus. In general, the myoclonic jerks are evocable by sudden sensory stimuli of all sorts (noise, bright light, touch), but they occur spontaneously as well. Twitches of individual ngers are typical but it should be emphasized that well-formed seizures are not a component of the illness. These changes gradually give way to a mute state, stupor, and coma, but the myoclonic contractions may continue to the end. Signs of degeneration of the pyramidal tracts or anterior horn cells, palsies of convergence and upgaze, and extrapyramidal signs occur in a small number of patients as the disease advances. The clinical diagnosis during life rests mostly on the recognition of one of the clusters of typical clinical features, particularly the unique syndrome of dementia which progresses much more quickly than that of common degenerative diseases coupled with stimulus-sensitive myoclonus and the characteristic EEG changes that occur in most patients (see below). The disease is invariably fatal, usually in less than a year from the onset. In about 10 percent of patients, the illness begins with almost stroke-like suddenness and runs its course rapidly, in a matter of a few weeks. At the other extreme, a small number of patients have reportedly survived for 2 to 10 years, but these cases should be accepted with caution; in some of them, SSE appears to have been superimposed on Alzheimer or Parkinson disease or some other chronic condition that predated the prion illness.
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Theta is the calculation of how the passage of time affects the price or premium of the option. If the Greeks are normalized in dollars as we have them in Figure 2.8, you can see the dollar amount that the options value will drop for each day that time passes. In Figure 2.8 the April 90 call has a theta of 6.87 meaning that the option will drop by $6.87 per day in time value. Note that the longer-term July 90 call option has a theta of 3.45, just over half the April option. The longer the term until expiration, the slower the time value decay. It is also important to notice that as you move farther away from the money, the theta tends to weaken as well. This is not a signi cant factor because the time decay is present on all the options. However, as a function of the overall value, the decay rate will be slightly slower.
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