Poison control

About: Poison control is a research topic. Over the lifetime, 394709 publications have been published within this topic receiving 15781638 citations.

Intimate Partner Violence as a Risk Factor for Mental Disorders: A Meta-Analysis

Abstract: This article reviews literature on the prevalence of mental health problems among women with a history of intimate partner violence. The weighted mean prevalence of mental health problems among battered women was 47.6% in 18 studies of depression, 17.9% in 13 studies of suicidality, 63.8% in 11 studies of posttraumatic stress disorder (PTSD), 18.5% in 10 studies of alcohol abuse, and 8.9% in four studies of drug abuse. These were typically inconsistent across studies. Weighted mean odds ratios representing associations of these problems with violence ranged from 3.55 to 5.62, and were typically consistent across studies. Variability was accounted for by differences in sampling frames. Dose-response relationships of violence to depression and PTSD were observed. Although research has not addressed many criteria for causal inferences, the existing research is consistent with the hypothesis that intimate partner violence increases risk for mental health problems. The appropriate way to conceptualize these problems deserves careful attention.

Epidemiology of trauma deaths: a reassessment

Abstract: OBJECTIVE: Recognizing the impact of the 1977 San Francisco study of trauma deaths in trauma care, our purpose was to reassess those findings in a contemporary trauma system. DESIGN: Cross-sectional. MATERIAL AND METHODS: All trauma deaths occurring in Denver City and County during 1992 were reviewed; data were obtained by cross-referencing four databases: paramedic trip reports, trauma registries, coroner autopsy reports and police reports. MEASUREMENTS AND MAIN RESULTS: There were 289 postinjury fatalities; mean age was 36.8 +/- 1.2 years and mean Injury Severity Score (ISS) was 35.7 +/- 1.2. Predominant injury mechanisms were gunshot wounds in 121 (42%), motorvehicle accidents in 75 (38%) and falls in 23 (8%) cases. Seven (2%) individuals sustained lethal burns. Ninety eight (34%) deaths occurred in the pre-hospital setting. The remaining 191 (66%) patients were transported to the hospital. Of these, 154 (81%) died in the first 48 hours (acute), 11 (6%) within three to seven days (early) and 26 (14%) after seven days (late). Central nervous system injuries were the most frequent cause of death (42%), followed by exsanguination (39%) and organ failure (7%). While acute and early deaths were mostly due to the first two causes, organ failure was the most common cause of late death (61%). CONCLUSIONS: In comparison with the previous report, we observed similar injury mechanisms, demographics and causes of death. However, in our experience, there was an improved access to the medical system, greater proportion of late deaths due to brain injury and lack of the classic trimodal distribution.

Threatened egotism, narcissism, self-esteem, and direct and displaced aggression: Does self-love or self-hate lead to violence?

Abstract: It has been widely asserted that low self-esteem causes violence, but laboratory evidence is lacking, and some contrary observations have characterized aggressors as having favorable self-opinions. In 2 studies, both simple self-esteem and narcissism were measured, and then individual participants were given an opportunity to aggress against someone who had insulted them or praised them or against an innocent third person. Self-esteem proved irrelevant to aggression. The combination of narcissism and insult led to exceptionally high levels of aggression toward the source of the insult. Neither form of self-regard affected displaced aggression, which was low in general. These findings contradict the popular view that low self-esteem causes aggression and point instead toward threatened egotism as an important cause.

The spectrum of disease in chronic traumatic encephalopathy

Abstract: Chronic traumatic encephalopathy is a progressive tauopathy that occurs as a consequence of repetitive mild traumatic brain injury. We analysed post-mortem brains obtained from a cohort of 85 subjects with histories of repetitive mild traumatic brain injury and found evidence of chronic traumatic encephalopathy in 68 subjects: all males, ranging in age from 17 to 98 years (mean 59.5 years), including 64 athletes, 21 military veterans (86% of whom were also athletes) and one individual who engaged in self-injurious head banging behaviour. Eighteen age- and gender-matched individuals without a history of repetitive mild traumatic brain injury served as control subjects. In chronic traumatic encephalopathy, the spectrum of hyperphosphorylated tau pathology ranged in severity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions, including the medial temporal lobe, thereby allowing a progressive staging of pathology from stages I-IV. Multifocal axonal varicosities and axonal loss were found in deep cortex and subcortical white matter at all stages of chronic traumatic encephalopathy. TAR DNA-binding protein 43 immunoreactive inclusions and neurites were also found in 85% of cases, ranging from focal pathology in stages I-III to widespread inclusions and neurites in stage IV. Symptoms in stage I chronic traumatic encephalopathy included headache and loss of attention and concentration. Additional symptoms in stage II included depression, explosivity and short-term memory loss. In stage III, executive dysfunction and cognitive impairment were found, and in stage IV, dementia, word-finding difficulty and aggression were characteristic. Data on athletic exposure were available for 34 American football players; the stage of chronic traumatic encephalopathy correlated with increased duration of football play, survival after football and age at death. Chronic traumatic encephalopathy was the sole diagnosis in 43 cases (63%); eight were also diagnosed with motor neuron disease (12%), seven with Alzheimer's disease (11%), 11 with Lewy body disease (16%) and four with frontotemporal lobar degeneration (6%). There is an ordered and predictable progression of hyperphosphorylated tau abnormalities through the nervous system in chronic traumatic encephalopathy that occurs in conjunction with widespread axonal disruption and loss. The frequent association of chronic traumatic encephalopathy with other neurodegenerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposition promote the accumulation of other abnormally aggregated proteins including TAR DNA-binding protein 43, amyloid beta protein and alpha-synuclein.