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In 60 children aged between two and 12 years the effect of rectal application of ketamine, dehydrobenzperiodol and atropine was investigated. The children were divided into two groups. Applying equal doses of dehydrobenzperidol and atropine, group B (30 children) received the half dose of ketamine which group A (30 children) received. This had a marked effect of preoperative salivation which was considerably less in group B. Using dehydrobenzperidol only 3.3% of the children vomited postoperatively. Sedation was satisfactory although especially the children in group B remained responsive, but were in a state of psychic indifference and motoric sedation. The applied combination of drugs effected a moderate reduction of heart rate. In general, we found that rectal application of 1 mg/kg ketamine, 0.15 mg/kg dehydrobenzperidol and 0.01 mg/kg atropine in children resulted in good preoperative sedation and exhibited relatively few side-effects.
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PMID:[Rectal premedication using ketamine-dehydrobenzperidol-atropine in childhood]. 227 47

The first central pharmacodynamic action of chlorpromazine to be described was sedation without narcosis. The antipsychotic action and extrapyramidal symptoms were observed later. Sedation can be separated into nonspecific sedation (drowsiness, somnolence) and specific sedation (psychomotor inhibition and psychic indifference). Both types are parts of the clinical profiles of classical neuroleptics. The sedative properties of neuroleptics may contribute to the overall efficacy in the treatment of psychotic patients, depending on the clinical situation. In most patients, however, sedation is only needed for a short period, or not at all. The drug induced sedation may adversely affect the patients' well-being and functional capabilities. The term neuroleptic-induced deficit syndrome (NIDS) has been coined to focus attention on the adverse mental effects of neuroleptics. NIDS still needs to be properly defined and to be differentiated from the deficit syndrome of schizophrenia and postpsychotic depression. Assessment methods are needed to establish the incidence and prevalence of NIDS, to evaluate the importance of NIDS in the overall treatment outcome in psychoses and to facilitate development of better antipsychotic agents.
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PMID:Neuroleptics and the neuroleptic-induced deficit syndrome. 791 56

Atypical antipsychotics will continue to be prescribed for the behavioral symptoms of dementia in the absence of more effective, better tolerated, and safer alternatives. The evidence base, although incomplete, suggests that modest treatment effect sizes are offset by risk of considerable adverse effects. How might this information be best applied to clinical practice? Non-pharmacologic strategies should be implemented in routine clinical practice. Placebo-controlled clinical trials of individual antipsychotic agents have historically reported high placebo response rates; CATIE-AD reported that the sum total of the risk/benefit equation of atypical antipsychotic therapy was no greater than that achieved by placebo. CATIE-AD was designed to study the effectiveness of atypical antipsychotic treatment in community dwelling patients with AD. It is uncertain whether the results can be generalized to the populations of dementia patients residing in nursing homes with more severe cognitive and behavioral impairment. There is some suggestion that nursing home patients with dementia complicated by severe behavioral symptoms, particularly agitation and aggression without accompanying psychosis, might achieve greater benefit from atypical antipsychotic treatment than patients with milder behavioral symptoms. The finding that dementia patients without psychosis may respond more robustly to antipsychotic treatment seems counterintuitive, but may support the hypothesis that the neurobiology of the "psychosis of AD" differs from the psychosis of schizophrenia or bipolar disease. Adverse effects associated with antipsychotic therapy should be aggressively monitored throughout therapy. Treatment-emergent sedation was associated with all of the atypical antipsychotics in CATIE-AD and is probably an important mediator of mortality risk in patients with dementia. Sedation exacerbates pre-existing cognitive impairment and increases the risk of complications such as aspiration pneumonia, so concomitant use of benzodiazepines should be discouraged or limited to short periods with careful observation.' Once initiated, the effectiveness and tolerability of antipsychotic therapy should be evaluated routinely. In Alzheimer's disease, the severity and frequency of behavioral symptoms often decreases as illness progresses. In a stable patient, it is prudent to attempt to taper and discontinue the antipsychotic after 2-8 months of therapy. Better understanding of the potential adverse effects of antipsychotic therapy has increased interest in the effects of the dementia-specific medications on behavioral symptoms. Reductions in neuropsychiatric symptoms have been reported from trials of individual cholinesterase inhibitors, memantine monotherapy, and memantine combined with donepezil in AD patients. Studies of small numbers of patients in open trials of cholinesterase inhibitors (donepezil, rivastigmine, galantamine) and one double-blind placebo controlled trial (rivastigmine) have reported varying degrees of improvement of behavioral symptoms and psychosis of dementia with Lewy bodies (DLB). Delusions, hallucinations, apathy, and agitation/aggression are cited as the symptom categories most likely to show significant improvement. Since few of these studies were prospectively designed to study behavioral symptoms, results must be interpreted cautiously. Treatment of behavioral symptoms in AD and other dementias is challenging. The limitations of current approaches drive the search for effective, well tolerated therapies.
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PMID:Atypical antipsychotics for the treatment of dementia-related behaviors: an update. 1763 94