Aggression and quantitative MRI measures of caudate in patients with chronic schizophrenia or schizoaffective disorder.

Nathan S. Kline Institute for Psychiatric Research, Orangeburg, NY 10962, USA.
Journal of Neuropsychiatry (Impact Factor: 2.77). 02/2006; 18(4):509-15. DOI: 10.1176/appi.neuropsych.18.4.509
Source: PubMed

ABSTRACT Caudate dysfunction is implicated in schizophrenia. However, little is known about the relationship between aggression and caudate volumes. Forty-nine patients received magnetic resonance imaging scanning in a double-blind treatment study in which aggression was measured. Caudate volumes were computed using a semiautomated method. The authors measured aggression with the Overt Aggression Scale and the Positive and Negative Syndrome Scale. Larger caudate volumes were associated with greater levels of aggression. The relationship between aggression and caudate volumes may be related to the iatrogenic effects of long-term treatment with typical antipsychotic agents or to a direct effect of schizophrenic processes on the caudate.

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    ABSTRACT: BACKGROUND: Haloperidol, used alone is recommended to help calm situations of aggression with people with psychosis. This drug is widely accessible and may be the only antipsychotic medication available in areas where resources are limited. OBJECTIVES: To investigate whether haloperidol alone, administered orally, intramuscularly or intravenously, is effective treatment for psychosis-induced agitation or aggression. SEARCH METHODS: We searched the Cochrane Schizophrenia Group Trials Register (1st June 2011). SELECTION CRITERIA: Randomised controlled trials (RCTs) involving people exhibiting agitation or aggression (or both) thought to be due to psychosis, allocated rapid use of haloperidol alone (by any route), compared with any other treatment. Outcomes included tranquillisation or asleep by 30 minutes, repeated need for rapid tranquillisation within 24 hours, specific behaviours (threat or injury to others/self), adverse effects. DATA COLLECTION AND ANALYSIS: We independently selected and assessed studies for methodological quality and extracted data. 'Summary of findings' tables were produced for each comparison grading the evidence and calculating, where possible and appropriate, a range of absolute effects. MAIN RESULTS: We included 32 studies comparing haloperidol with 18 other treatments. Few studies were undertaken in circumstances that reflect real world practice, and, with notable exceptions, most were small and carried considerable risk of bias.Compared with placebo, more people in the haloperidol group were asleep at two hours (2 RCTs, n = 220, risk ratio (RR) 0.88, 95% confidence interval (CI) 0.82 to 0.95). Dystonia was common (2 RCTs, n = 207, RR 7.49, CI 0.93 to 60.21). Compared with aripiprazole, people in the haloperidol group required fewer injections than those in the aripiprazole group (2 RCTs, n = 473, RR 0.78, CI 0.62 to 0.99). More people in the haloperidol group experienced dystonia (2 RCTs, n = 477, RR 6.63, CI 1.52 to 28.86).Despite three larger trials with ziprasidone (total n = 739), data remain patchy, largely because of poor design and reporting. Compared with zuclopenthixol acetate, more people who received haloperidol required more than three injections (1 RCT, n = 70, RR 2.54, CI 1.19 to 5.46).Three trials (n = 205) compared haloperidol with lorazepam. There were no significant differences between the groups with regard to the number of participants asleep at one hour (1 RCT, n = 60, RR 1.05, CI 0.76 to 1.44). However, by three hours, significantly more people were asleep in the lorazepam group compared with the haloperidol group (1 RCT, n = 66, RR 1.93, CI 1.14 to 3.27). There were no differences in numbers requiring more than one injection (1 RCT, n = 66, RR 1.14, CI 0.91 to 1.43).Haloperidol's adverse effects were not offset by addition of lorazepam (e.g. dystonia 1 RCT, n = 67, RR 8.25, CI 0.46 to 147.45; required antiparkinson medication RR 2.74, CI 0.81 to 9.25). Addition of promethazine was investigated in one larger and better graded trial (n = 316). More people in the haloperidol group were not tranquil or asleep by 20 minutes (RR 1.60, CI 1.18 to 2.16). Significantly more people in the haloperidol alone group experienced one or more adverse effects (RR 11.28, CI 1.47 to 86.35). Acute dystonia for those allocated haloperidol alone was too common for the trial to continue beyond the interim analysis (RR 19.48, CI 1.14 to 331.92). AUTHORS' CONCLUSIONS: If no other alternative exists, sole use of intramuscular haloperidol could be life-saving. Where additional drugs to offset the adverse effects are available, sole use of haloperidol for the extreme emergency, in situations of coercion, could be considered unethical. Addition of the sedating promethazine has support from better-grade evidence from within randomised trials. Use of an alternative antipsychotic drug is only partially supported by fragmented and poor-grade evidence. Evidence for use of newer generation antipsychotic alternatives is no stronger than that for older drugs. Adding a benzodiazepine to haloperidol does not have strong evidence of benefit and carries a risk of additional harm.After six decades of use for emergency rapid tranquillisation, this is still an area in need of good independent trials relevant to real world practice.
    Cochrane database of systematic reviews (Online) 01/2012; 11(11):CD009377. DOI:10.1002/14651858.CD009377.pub2 · 5.94 Impact Factor
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    ABSTRACT: How to cite this article: E. Zampieri, M. Bellani, B. Crespo-Facorro and P. Brambilla Basal ganglia anatomy and schizophrenia: the role of antipsychotic treatment. Epidemiology and Psychiatric Sciences, Available on CJO 2014 This Section of Epidemiology and Psychiatric Sciences regularly appears in each issue of the Journal to stress the relevance of epidemiology for behavioral neurosciences, reporting the results of studies that explore the use of an epidemiological approach for providing a better understanding of the neural basis of major psychiatric disorders and, in turn, the utilisation of the behavioural neurosciences for promoting innovative epidemiological research. The final scope is to help the translation of most relevant research findings into everyday clinical practice. These contributions are written in house by the journal's editorial team or commissioned by the Section Editor (no more than 1000 words, short unstructured abstract, 4 keywords , one Table or Figure and up to ten references). Paolo Brambilla, Section Editor
    Epidemiology and Psychiatric Sciences 11/2014; · 3.36 Impact Factor
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    ABSTRACT: People with schizophrenia are at increased risk, as compared to the general population, to acquire convictions for violent crimes and homicide. They also show elevated levels of aggressive behaviour. While psychotic symptoms explain aggressive behaviour that is common during acute episodes, they do not explain such behaviour at other stages of illness or prior to illness onset. Three distinct phenotypes have been identified: individuals with a childhood onset of conduct disorder who display antisocial and aggressive behaviour both before and after schizophrenia onset; individuals with no history of conduct problems who begin engaging in aggressive behaviour as illness onsets; and individuals who after many years of illness engage in a severe physical assault. Little is known about the aetiology aetiology of the three types of offenders and about the neural mechanisms that initiate and maintain these behaviours. We hypothesize that schizophrenia preceded by conduct disorder is associated with a combination of genes conferring vulnerability for both disorders and altering the effects of environmental factors on the brain, and thereby, with a distinct pattern of neural development. Some evidence is available to support this hypothesis. By contrast, offending among adults with schizophrenia schizophrenia who have no history of such behaviour prior to illness may result from the changes in the brain that occur as illness onsets, and that are further altered by comorbid conditions such as substance misuse, or by the progressive changes in the brain through adulthood that may result from the illness and from the use of antipsychotic medications.
    12/2013; DOI:10.1007/7854_2013_259

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