Delirium occurs at rates ranging from 10% to 30% of all hospital admissions. It is a negative prognostic indicator, often leading to longer hospital stays and higher mortality. The aetiology of delirium is multifactorial and many causes have been suggested. The stress-diathesis model, which posits an interaction between the underlying vulnerability and the nature of the precipitating factor, is useful in understanding delirium. Preventing delirium is the most effective strategy for reducing its frequency and complications. Environmental strategies are valuable but are often underutilized, while remedial treatment is usually aimed at specific symptoms of delirium. Antipsychotics are the mainstay of pharmacological treatment and have been shown to be effective in treating symptoms of both hyperactive and hypoactive delirium, as well as generally improving cognition. Haloperidol is considered to be first-line treatment as it can be administered via many routes, has fewer active metabolites, limited anticholinergic effects and has a lower propensity for sedative or hypotensive effects compared with many other antipsychotics. Potential benefits of atypical compared with typical antipsychotics include the lower propensity to cause over-sedation and movement disorder. Of the second-generation antipsychotics investigated in delirium, most data support the use of risperidone and olanzapine. Other drugs (e.g. aripiprazole, quetiapine, donepezil and flumazenil) have been evaluated but data are limited. Benzodiazepines are the drugs of choice (in addition to antipsychotics) for delirium that is not controlled with an antipsychotic (and can be used alone for the treatment of alcohol and sedative hypnotic withdrawal-related delirium). Lorazepam is the benzodiazepine of choice as it has a rapid onset and shorter duration of action, a low risk of accumulation, no major active metabolites and its bioavailability is more predictable when it is administered both orally and intramuscularly.
Paliperidone palmitate was effective and well tolerated in this naturalistic cohort. Optimising treatment by targeting PP for patients identified as having lower risk of discontinuation can give rise to continuation rates approaching 80% at 1 year.
BackgroundVisual hallucinations occur in various neurological diseases, but are most prominent in Lewy body dementia, Parkinson's disease and schizophrenia. The lifetime prevalence of visual hallucinations in patients with schizophrenia is much more common than conventionally thought and ranges from 24% to 72%. Cortical acetylcholine (ACh) depletion has been associated with visual hallucinations; the level of depletion being related directly to the severity of the symptoms. Current understanding of neurobiological visual processing and research in diseases with reduced cholinergic function, suggests that AChEI's may prove beneficial in treating visual hallucinations. This offers the potential for targeted drug therapy of clinically symptomatic visual hallucinations in patients with schizophrenia using acetylcholinesterase inhibition.MethodsA systematic review was carried out investigating the evidence for the effects of AChEI's in treating visual hallucinations in Schizophrenia.ResultsNo evidence was found relating to the specific role of AChEI's in treating visual hallucinations in this patient group.DiscussionGiven the use of AChEI's in targeted, symptom specific treatment in other neuropsychiatric disorders, it is surprising to find no related literature in schizophrenia patients. The use of AChEI's in schizophrenia has investigated effects on cognition primarily with non cognitive effects measured more broadly.ConclusionsWe would suggest that more focused research into the effects of AChEI's on positive symptoms of schizophrenia, specifically visual hallucinations, is needed.
Real-world, effectiveness studies add an important new dimension to the evaluation of the benefits of individual antipsychotics. Efficacy studies have already shown the unique effectiveness of clozapine, and suggested improved outcomes for olanzapine compared with some atypical antipsychotics and a reduced tendency to produce acute and chronic movement disorders for atypical compared with typical drugs. Recent effectiveness studies largely confirm these prior observations. The CATIE (Clinical Antipsychotic Trials of Intervention Effectiveness), CUtLASS (Cost Utility of the Latest Antipsychotic Drugs in Schizophrenia Study) and SOHO (Schizophrenia Outpatient Health Outcomes) programmes confirmed the superiority of clozapine over other antipsychotics; CATIE and SOHO also confirmed olanzapine as probably the second most effective antipsychotic. Effectiveness studies have confirmed the high incidence of adverse metabolic effects with clozapine, olanzapine and (with less certainty) quetiapine but the ZODIAC (Ziprasidone Observational Study of Cardiac Outcomes) study found no excess cardiovascular events or deaths for olanzapine compared with ziprasidone. Prior observations on reduced frequency of movement disorders for second-generation versus first-generation antipsychotics were also largely (but not uniformly) supported. Overall, recent real-world studies have done much to confirm prior observations from efficacy-based randomized, controlled trials.
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