Childhood neurodevelopmental markers and risk of premature mortality: Follow-up to age 60-65 years in the Aberdeen Children of the 1950s study.

BACKGROUND: Individual neurodevelopmental disorders are associated with premature mortality. Little is known about the association between multiple neurodevelopmental markers and premature mortality at a population level. The ESSENCE (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations) approach considers multiple neurodevelopmental parameters, assessing several markers in parallel that cluster, rather than considering individual diagnostic categories in isolation. OBJECTIVES: To determine whether childhood neurodevelopmental markers, including reduced intellectual functioning, are associated with all-cause premature mortality. METHODS AND PROCEDURES: In a general population cohort study (n = 12,150) with longitudinal follow up from childhood to middle age, Cox proportional hazard models were used to study the associations between childhood neurodevelopmental markers (Rutter B scale and IQ) and premature all-cause mortality. OUTCOMES AND RESULTS: The cognitive measures and 21 of the 26 Rutter B items were significantly associated with premature mortality in bivariate analyses with hazard ratios from 1.24 (95% CI 1.05-1.47) to 2.25 (95% CI 1.78-2.90). In the final adjusted model, neurodevelopmental markers suggestive of several domains including hyperactivity, conduct problems and intellectual impairment were positively associated with premature mortality and improved prediction of premature mortality. CONCLUSIONS: A wide range of neurodevelopmental markers, including childhood IQ, were found to predict premature mortality in a large general population cohort with longitudinal follow up to 60-65 years of age. IMPLICATIONS: These findings highlight the importance of a holistic assessment of children with neurodevelopmental markers that addresses a range of neurodevelopmental conditions. Our findings could open the door to a shift in child public mental health focus, where multiple and/or cumulative markers of neurodevelopmental conditions alert clinicians to the need for early intervention. This could lead to a reduction in the risk of broad health outcomes at a population level.

Mortality in individuals with disruptive behavior disorders diagnosed by specialist services - A nationwide cohort study.

Disruptive behavior disorders (DBDs), inclusive of oppositional defiant disorder (ODD) and conduct disorder (CD), are associated with outcomes likely to increase risk of mortality. Using Danish National Registers, a total of 1.92 million individuals including 9495 individuals with DBDs diagnosed by specialist services were followed from their first birthday to 2013. Those with and without DBDs were compared using mortality rate ratios (MRRs) estimated using Poisson regression and adjusted for calendar period, age, sex, family history of psychiatric disorders, maternal age at time of birth, paternal age at time of birth, parental education status, and parental employment status. Over the course of follow up, which totalled 24.9 million person-years, 5580 cohort members died including 78 individuals with DBDs. The mortality rate per 10,000 person-years was 9.66 for individuals with DBDs compared to 2.22 for those with no diagnosis. This corresponded to a fully adjusted MRR of 2.57 (95% confidence interval 2.04-3.20). Comorbid substance use disorder and attention-deficit/hyperactivity disorder resulted in the highest MRR across all categories. These findings demonstrate the excess mortality associated with DBDs.

Adolescent conduct problems and premature mortality: follow-up to age 65 years in a national birth cohort.

BACKGROUND: Severe youth antisocial behaviour has been associated with increased risk of premature mortality in high-risk samples for many years, and some evidence now points to similar effects in representative samples. We set out to assess the prospective association between adolescent conduct problems and premature mortality in a population-based sample of men and women followed to the age of 65 years. METHOD: A total of 4158 members of the Medical Research Council National Survey of Health and Development (the British 1946 birth cohort) were assessed for conduct problems at the ages of 13 and 15 years. Follow-up to the age of 65 years via the UK National Health Service Central Register provided data on date and cause of death. RESULTS: Dimensional measures of teacher-rated adolescent conduct problems were associated with increased hazards of death from cardiovascular disease by the age of 65 years in men [hazard ratio (HR) 1.17, 95% confidence interval (CI) 1.04-1.32], and of all-cause and cancer mortality by the age of 65 years in women (all-cause HR 1.16, 95% CI 1.07-1.25). Adjustment for childhood cognition and family social class did little to attenuate these risks. Adolescent conduct problems were not associated with increased risks of unnatural/substance-related deaths in men or women in this representative sample. CONCLUSIONS: Whereas previous studies of high-risk delinquent or offender samples have highlighted increased risks of unnatural and alcohol- or substance abuse-related deaths in early adulthood, we found marked differences in mortality risk from other causes emerging later in the life course among women as well as men.

[Recognition and treatment of behavioral and psychological symptoms of dementias: lessons from the CATIE-AD study]. / Demenciákhoz társuló viselkedési és pszichés zavarok felismerése és kezelése antipszichotikumokkal: a CATIE-AD vizsgálat tanulságai.

The prevalence of the behavioral and psychological symptoms of dementia (BPSD) varies between 20-90%, depending on the care settings and severity of the dementia syndrome. BPSD is the major reason for referrals to secondary care. It exacerbates the dementia-associated morbidity and mortality rates. Furthermore, while BPSD is not a properly defined syndrome, it frequently induces psychic and somatic complaints in caregivers. The social and economic impacts of the BPSD far outweigh the importance of the cognitive symptoms of dementia. The aim of this review is to present the most recent findings regarding the recognition, differential diagnosis, aetiology, and pathomechanism of BPSD with a special focus on the local therapeutic possibilities with the atypical antipsychotics. Of utmost importance is the process of identifying the complex bio-psycho-social aetiological factors in parallel with defining the treatment strategies. Only after the correct recognition of the potential aetiology, non-pharmacological interventions are recommended to start with as first choice treatment in mild and mild-to-moderate BPSD, while in moderate and severe cases pharmacotherapeutic approaches are recommended from the start. Recent findings of neuropathological, neurochemical and neuroimaging studies yielded unequivocal evidence that the BPSD symptoms are not a consequence of a single neurotransmitter imbalance, but rather of disproportionate level changes in biogenic amines, excitatory and inhibitory transmitters in the central nervous system. Consequently, the available pharmacotherapy should target the balancing of the dopaminergic, serotoninergic, noradrenergic, excitatory and GABAergic neurotransmission by using antipsychotics, antidepressants, phase-prophylactic agents, and benzodiazepines. Several clinical studies have proven the efficacy of atypical antipsychotics that target multiple neurotransmitter systems in treating BPSD. The first results of the CATIE-AD study also confirm these findings and indicate that the atypical antipsychotics are effective in controlling anger, aggression and delusions in Alzheimer's disease, while cognitive symptoms, quality of life and care needs are not improved.