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Assessment Scales Before any intervention is initiated, observation and documentation of the level of disturbance should be performed with the help of well-established instruments to measure the severity and frequency of the symptoms. This assessment can be repeated over time to determine the efficacy of the intervention. To determine the level of existing cognitive impairment, 2 commonly used tools are the Mini-Mental State Examination21 and Dementia Rating Scale.22 The Mini-Mental State Examination is a 30-point scale developed to detect the presence of cognitive impairment, with a score lower than 23 indicating impairment. The Dementia Rating Scale is a 144-point scale developed to assess dementia, with a score lower than 123 indicating impairment.22 Measures used to describe and monitor behavioral symptoms in older or demented persons are numerous. Examples of instruments include the Neuropsychiatric Inventory, 23 Geriatric Depression Scale, 24 and CohenMansfield Agitation Inventory.25 The Neuropsychiatric Inventory consists of 10 domains with total scores ranging from 0 to 120. Psychiatrically healthy controls score 0.26 The Geriatric Depression Scale consists of 30 questions, with a total possible score of 30. Scores higher than 9 are considered clinically important.27 The Cohen-Mansfield Agitation Inventory measures agitated behaviors recorded by caregivers. This instrument is designed for the assessment of nursing home residents and elderly persons living in a community.25 BEHAVIORAL ASSESSMENT AND MANAGEMENT APPROACHES Behavior: A Key Form of Communication Communication is adaptive for all people, generally a means toward need fulfillment. When language and reasoning are limited, communication is likely to be more overtly behavioral. In a young child, crying as a means of communicating hunger, pain, or fear is not considered a "behavior problem." In patients with dementia, as reasoning and language skills are lost, behavior will increasingly become a primary form of communication. Even when speech is intact, verbal communication is often limited by difficulties in expressing desired thoughts correctly. The behavior of patients with dementia often represents an attempt to express feelings and needs that cannot be verbalized adequately. Labeling of unwanted behaviors as "bad" or "difficult" negates the adaptation that may be inherent in the behavior. Such labeling can foster a sense of futility or resignation. Patients with dementia typically lack the cognitive skill to be manipulative with their behaviors. Rather, behavioral problems arise from the disease process and the resulting primitive coping and communication styles.15 and
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FIG. 2. Transactivation in Ishikawa cells stably expressing human ERa Ishikawa-hERa ; or ERb Ishikawa-hERb ; : Agonistic activity of phytoestrogens. A and B ; Ishikawa-hERa or C and D ; Ishikawa-hERb cells were transiently transfected with 3 ERE-Luc and pRL-CMV. Following transfection, cells were treated with each compound at the indicated concentrations for 22 h. Each value was normalized to the internal luciferase control and results are expressed as the fold induction compared to the solvent control. The dotted line indicates the value of the solvent control set to 1 ; . Each data point represents the average with range of duplicate determinations. Experiments were performed at least three times with reproducible results and
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There is general consensus that the sooner any treatment is started, the better the prognosis. This may be related to the rate of spontaneous remissions or to a better response in early stage of the disease. These questions are also still not answered. A prediction of the final recovery seems to be possible from the therapeutic result after 7 days of any given treatment 24. There is probably few other disease for which such a variety of treatments have been proposed, and still today, many different treatment regimens, some more invasive than others, are propagated 25 26 27 Their therapeutic efficacy is very difficult to establish. It seems however, that the therapeutic outcome of several proposed drug treatment regimes is in the same range as the spontaneous recovery rate, which itself is still the subject of controversy. This is the result of several double-blind prospective trials, where no advantage over NaCl infusion could be established19 29. A significant improvement vs. placebo therapy could however be observed with high-dose intravenous corticosteroid treatment in a degressive scheme 21, as well as with hemodiluton therapy in patients with an increased haematocrit above 44% ; 30. As these effects have not been reproduced equivocally by other authors, these therapeutic options have not become "accepted standard" in ENT. In fact, not one drug treatment regimen has gained universal acceptance in ENT. The efficacy of HBO for sudden deafness has not been conclusively established. Experimental research proves the increase of oxygen partial pressure in the inner ear and the improvement of the function under this condition31. Retrospectively, a large meta-analysis by Lamm et al. 1998 ; 25 showed a positive effect of HBO in approximately 50% of cases, after failure of classical drug therapy. It was noted however that there was a very large variability in the nature and duration of the classical drug therapy administered prior to HBO. This is to be considered a weakness of these retrospective studies. A french study 32 compared HBO vasodilator corticotherapy to vasodilator corticotherapy alone and to haemodilution therapy. Although the HBO group scored better, the results were not significant. There have been few prospective studies. Most of these studies initiated therapy as soon as possible after the onset of deafness, thereby including the large number of patients who would recover spontaneously, no matter how or even if treated. Pilgramm et al.33, comparing 37 patients, treated with haemodilution with or without HBO, showed a similar, not significant advantage of adjuvant HBO. Flunkert et al. 200034 compared haemodilutive and HBO as a first treatment in early stages of the disease in a prospective controlled trial and saw equal outcome with insignificant advantages for HBO. Many other prospective studies are only presented as communications on HBO congresses, and are never published in peer-reviewed papers. In summary, there appears to be a need for a large prospective clinical trial to clearly establish the place of HBO in the treatment of SD.
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710. Ninane J, Grymonprez A, Burtonboy G, Franois A, Cornu G. Disseminated BCG in HIV infection. Arch Dis Child 1988; 63: 1268-9. Lallemant-Le Coeur S, Lallemant M, Cheynier D, Nzingoula S, Drucker J, Larouz B. Bacillus Calmette-Gurin immunization in infants born to HIV-1seropositive mothers. AIDS 1991; 5: 195-9. Besnard M, Sauvion S, Offredo C, Gaudelus J, Gaillard JL, Veber F, Blanche S. Bacillus Calmette-Gurin infection after vaccination of human immunodeficiency virus-infected children. Pediatr Infect Dis 1993; 12: 993-7. Rosenfeldt V, Prregaard A, Valerius NH. Disseminated infection with Bacillus Calmette-Guerin in a child with advanced HIV disease. Scand J Infect Dis 1997; 29: 526-7. Romanus V, Fasth A, Tordai P, Wiholm BE. Adverse reactions in healthy and immunocompromised children under six years of age vaccinated with the Danish BCG vaccine, strain Copenhagen 1331: implications for the vaccination policy in Sweden. Acta Paediatr 1993; 82: 1043-52. van Deutekom H, Smulders YM, Roozendaal KJ, van Soolingen D. Bacille Calmette-Gurin BCG ; meningitis in an AIDS patient 12 years after vaccination with BCG. Correspondence ; . Clin Infect Dis 1996; 22: 870-1. O'Brien KL, Ruff AJ, Louis MA, Desormeaux J, Joseph DJ, McBrien M, Coberly J, Boulos R, Halsey NA. Bacillus Calmette-Gurin complications in children born to HIV-1-infected women with a review of the literature. Pediatrics 1995; 95: 414-8. Reynes J, Perez C, Lamaury I, Janbon F, Bertrand A. Bacille Calmette-Gurin adenitis 30 years after immunization in a patient with AIDS. Correspondence ; . J Infect Dis 1989; 160: 727. Armbruster C, Junker W, Vetter N, Jaksch G. Disseminated Bacille CalmetteGurin infection in an AIDS patient 30 years after BCG vaccination. Correspondence ; . J Infect Dis 1990; 162: 1216. Reichman LB. Why hasn't BCG proved dangerous in HIV-infected patients? JAMA 1989; 261: 3246. Waddell RD, Lishimpi K, Fordham von Reyn C, Chintu C, Baboo KS, Kreiswirth B, Talbot EA, Karagas MR. Bacteremia due to Mycobacterium tuberculosis or M. bovis, Bacille Calmette-Gurin BCG ; among HIV-positive children and adults in Zambia. AIDS 2001; 15: 55-60. World Health Organization. Special Programme on AIDS and Expanded Programme on Immunization Joint Statement. Consultation on human immunodeficiency virus HIV ; and routine childhood immunization. WHO Wkly Epidem Rec 1987; 62: 297-9. Milstien JB, Gibson JJ. Quality control of BCG vaccine by WHO: a review of factors that may influence vaccine effectiveness and safety. Bull World Health Organ 1990; 68: 93-108.
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