Television and aggression: a test of a mediated model with a sample of Portuguese students

We examined the role of identification with violent TV heroes, enjoyment of TV violence, and perceived reality in TV violence as mediators of the relationship between viewing TV violence and subsequent physical and verbal aggression. A sample of 722 4th, 6th, and 8th grade students from schools in the central region of Portugal completed measures assessing enjoyment of TV violence, perceived reality, aggression, identification with violent TV heroes, and exposure to TV violence. The results showed that the relationship between TV violence and physical aggression is mediated by enjoyment of TV violence, perceived reality in TV violence, and identification with violent TV heroes. The TV violence to verbal aggression relationship was also mediated by enjoyment of TV violence.     

Inconsistencies in the Reporting of Perceived Trauma Severity Among Acute Physical Injury Survivors

This study aimed to identify and predict inconsistency in perceived trauma severity reports over time among trauma survivors. Hospitalized adult survivors of a traumatic injury completed trauma exposure assessments within 40 days post-injury and 6 weeks later (n = 77). The following trauma severity characteristics were examined: (1) threat of loss of life, (2) threat of loss of a body part, (3) threat of serious injury, and (4) peritraumatic emotionality. Potential predictors of inconsistency were also examined. About half of the reports regarding perceived trauma severity characteristics were inconsistent between the baseline to 6-week assessment. The inconsistent reports were mostly small and equally likely to be either more or less severe over time. Increases in posttraumatic stress disorder (PTSD; especially avoidance) predicted increases in severity of life threat and threat of loss of a body part. Thus, acute reports of perceived trauma severity vary and are influenced by PTSD symptoms.     

The Processing of Grammatical Gender Agreement in Brazilian Portuguese: ERP Evidence in Favor of a Single Route

Journal of Psycholinguistic Research - The present study used event-related potentials to investigate whether the processing of grammatical gender agreement involving gender regular and irregular...     

Confirmation of an Inhibitory Control Deficit in Attention-Deficit/Hyperactivity Disorder

The objective of this study was to determine whether deficient inhibitory control distinguishes children with a diagnosis of attention-deficit/hyperactivity (ADHD) disorder, conduct disorder (CD), and comorbid ADHD + CD from normally developing children. Participants were rigorously diagnosed children (age 7 to 12 years) with ADHD (N = 72), CD (N = 13) or ADHD + CD (N = 47) and 33 control children (NC). We studied inhibitory control using the stop-signal paradigm, a laboratory task that assessed the ability to inhibit an ongoing action. The ADHD group had significantly impaired inhibitory control compared to NC, CD, and ADHD + CD children. These results indicate that children with ADHD have deficient inhibition as measured in the stop-signal paradigm and that ADHD occurring in the presence of ADHD + CD may represent a phenocopy of CD rather than a variant of ADHD.     

The role of a lifetime history of oppositional defiant and conduct disorders in adults with ADHD: implications for clinical practice

IntroductionAttention-deficit/hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), and conduct disorder (CD) are frequently co-occurring disorders in children and adolescents. However, their clinical status among adults is still under discussion. This study analyzes how the current clinical presentation of adult ADHD might be influenced by a lifetime history of CD and ODD. METHODS: We compared three groups of patients: ADHD without history of CD/ODD (n = 178), ADHD + history of ODD (n = 184), and ADHD + history of CD (n = 96). RESULTS: A history of CD (and to a lower extent ODD) is associated with a more severe and externalizing profile.ConclusionPast CD and ODD entail a significant negative mental health impact on persistent ADHD, reinforcing the importance of actively assessing the developmental history of adult ADHD patients.     

Stress, Glucocorticoids, and Damage to the Nervous System: The Current State of Confusion

An extensive literature demonstrates that glucocorticoids (GCs), the adrenal steroids secreted during stress, can have a broad range of deleterious effects in the brain. The actions occur predominately, but not exclusively, in the hippocampus, a structure rich in corticosteroid receptors and particularly sensitive to GCs. The first half of this review considers three types of GC effects: a) GC-induced atrophy, in which a few weeks' exposure to high GC concentrations or to stress causes reversible atrophy of dendritic processes in the hippocampus; b) GC neurotoxicity where, over the course of months, GC exposure kills hippocampal neurons; c) GC neuroendangerment, in which elevated GC concentrations at the time of a neurological insult such as a stroke or seizure impairs the ability of neurons to survive the insult. The second half considers the rather confusing literature as to the possible mechanisms underlying these deleterious GC actions. Five broad themes are discerned: a) that GCs induce a metabolic vulnerability in neurons due to inhibition of glucose uptake; b) that GCs exacerbate various steps in a damaging cascade of glutamate excess, calcium mobilization and oxygen radical generation. In a review a number of years ago, I concluded that these two components accounted for the deleterious GC effects. Specifically, the energetic vulnerability induced by GCs left neurons metabolically compromised, and less able to carry out the costly task of containing glutamate, calcium and oxygen radicals. More recent work has shown this conclusion to be simplistic, and GC actions are shown to probably involve at least three additional components: c) that GCs impair a variety of neuronal defenses against neurologic insults; d) that GCs disrupt the mobilization of neurotrophins; e) that GCs have a variety of electrophysiological effects which can damage neurons. The relevance of each of those mechanisms to GC-induced atrophy, neurotoxicity and neuroendangerment is considered, as are the likely interactions among them.