Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As clinicians we talk about "the best interests of our patients". How can a treatment which doubles the rate of cognitive decline, triples the rate of stroke, doubles mortality, substantially increases falls and fractures and reduces quality of life be beneficial, especially, as in real life, once neuroleptics are started they are rarely discontinued with cumulative adverse effects? As there is clearly no rational reason for prescribing, we need to consider other explanations. We would suggest the following: Therapeutic impotence: Doctors, especially specialists feel they need to do something, and prescribing a familiar drug is the easiest option. Ignorance: Doctors are either unaware of the substantial evidence of harm with neuroleptics or are swayed by slick marketing information, portraying atypical neuroleptics in an "over-safe" light that does not reflect the actual data. Placebo effect: If neuroleptics are prescribed, the majority of patients experience an improvement in BPSD symptoms. This reinforces the apparent value of this practice, as we like to take the credit for any improvements that occur. The reality is that the majority of people would have experienced a comparable improvement with monitoring. Bowing to pressure: Sometimes the pressure to respond can be great, and a prescription is an easy way to relieve the pressure. This is understandable, and reflects a similar phenomenon to that of general practioners prescribing antibiotics for sore throats. In neither situation does it represent good practice. Lack of skills to implement non-pharmacological alternatives: The main evidence for alternative treatment options are for therapies that by and large are not a core part of the physician or psychiatrist's skill-base, such as psychological interventions. Doctors therefore feel uncomfortable pursuing these options. Why for example is so little time spent on the nonpharmacological interventions that everyone agrees should be the first line of treatment for BPSD in people with dementia? It is largely assumed that the "enlightened clinician has already appropriately assessed and diagnosed the patient and exhausted all the possible environmental and behavioral interventions before resorting to the prescription pad." Accumulating evidence clearly indicates that the need for psychotropic medication is substantially reduced by proactive services or interventions which can provide training and promote psychological, social and environmental and sensory interventions. The prescription but is an easy but not an acceptable alternative. Over-adherence to prescribing guidance: There are pharmacological alternatives to neuroleptics if a prescription is needed. Although the evidence for the more promising alternatives needs to be developed much further, drugs such as cholinesterase inhibitors may offer a much less harmful alternative. The reluctance of clinicians to use cholinesterase inhibitors in this way is puzzling, and presumably is because of the culture of "guidance-prescribing" that has evolved around these agents. If the treatment of BPSD is to move forward, we need to challenge the way we have always done things, examine the evidence and move forward with new and flexible multi-disciplinary approaches if we are truly to look after the "best interests of our patients".
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PMID:Drugs used to relieve behavioral symptoms in people with dementia or an unacceptable chemical cosh? Argument. 1594 89

The objective was to compare survival in a population-based cohort of elderly demented patients with behavioural and psychological symptoms (BPSD) dispensed an atypical antipsychotic (AA) with that of a sample of demented patients not treated with AAs. An observational cohort study was carried out in the province of Modena, Italy (644,000 inhabitants) on a cohort of 294 patients with BPSD diagnosed by a dementia specialist and treated with an AA, and a cohort of 2020 demented adults not dispensed AAs. All patients were 65 years of age or older. Measured outcomes were death by any cause and death by cerebrovascular accident at the end of the study. After a median follow-up of one year, survival was not significantly different between patients treated and not treated with AAs (overall mortality rates: 0.52 vs. 0.55/1000 years/person, respectively; relative risk reduction 0.047, 95% confidence interval -0.251 to 0.286). Multivariate survival analysis showed that older age at entry, male gender, severe dementia and functional impairment were associated with a higher risk of death. Although our sample size does not allow the exclusion of small differences in the short term, age, gender and dementia severity but not treatment with AAs seem to influence survival among elderly demented patients.
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PMID:Survival among elderly Italian patients with dementia treated with atypical antipsychotics: observational study. 1720 22