No abstract

Assessing emotional dynamics in the brain offers insight into the fundamental neural and psychological mechanisms underlying emotion. One such dynamic is emotional inertia—the influence of one’s emotional state at one time point on one’s emotional state at a subsequent time point. Emotion inertia reflects emotional rigidity and poor emotion regulation as evidenced by its relationship to depression and neuroticism. In this study, we assessed changes in cerebral blood flow (CBF) from before to after an emotional task and used these changes to predict stress, positive and negative emotional inertia in daily life events. Cerebral blood flow changes in the lateral prefrontal cortex (lPFC) predicted decreased non-specific emotional inertia, suggesting that the lPFC may feature a general inhibitory mechanism responsible for limiting the impact that an emotional state from one event has on the emotional state of a subsequent event. CBF changes in the ventromedial prefrontal cortex and lateral occipital cortex were associated with positive emotional inertia and negative/stress inertia, respectively. These data advance the blossoming literature on the temporal dynamics of emotion in the brain and on the use of neural indices to predict mental health-relevant behavior in daily life.

Background Genetic influences on stress reactivity may provide insight into depression risk mechanisms. The C-allele of rs6318, a putatively functional polymorphism located within the HTR2C gene, has been reported to predict greater cortisol and negative affective reactivity to lab-induced stress. However, the potential moderating effect of sex has not been examined despite X-linkage of HTR2C. We hypothesized that sex moderates the effect of rs6318 on cortisol and affective reactivity to lab-induced stress, with males showing stronger effects. Methods Non-depressed young adults (N = 112; 39 female) screened via clinical interview provided a DNA sample and completed either a negative evaluative Trier Social Stress Test, or a non-evaluative control protocol. Salivary cortisol and self-reported affect were assessed at four timepoints. Results Contrary to hypotheses, C-carriers showed blunted rather than exaggerated cortisol responses to lab-induced stress in multilevel models (b = 0.467, p < 0.001), which persisted when covarying subclinical depression symptoms. This effect was not moderated by sex (b = 0.174, p = 0.421), and remained significant when examining females (b = 0.362, p = 0.013) and males (b = 0.537, p < 0.001) separately. C-carriers also exhibited marginally greater reactivity in negative self-focused affect in response to stress than non-carriers when covarying subclinical depression symptoms (b = −0.360, p = 0.067), and exhibited higher levels of subclinical depression symptoms than non-carriers (F = 6.463, p = 0.012). Conclusions Results support a role for the rs6318 C-allele in dysregulated stress responding, and suggest that the C-allele may contribute to risk for depression.

No abstract

Introduction: Switching from immediate release Methylphenidate (MPH-IR) to a sustained release formulation of MPH-IR in the treatment of ADHD is often required to provide better compliance and convenience; however switch was reported to be not always successful. Objective: Small doses of MPH-IR may be added to sustained release preparations when its effect wears off. Aims/Method: Clinical case notes of 77 subjects aged 6-18 years who had been switched from MPH-IR to Concerta XL (an osmotic controlled-release formulation (OROS) of MPH) were retrospectively analysed for the effectiveness of the switch and the impact of an extra mid-afternoon dose of MPH-IR on the outcome. Results: Switch to Concerta XL alone was successful in 94% of cases and all 23 (100%) subjects who had MPH-IR added to Concerta XL showed good response to switch. More than 43% of patients required late afternoon top-up with MPH-IR to make a successful switch whilst 55% of patients required a larger dose of Concerta XL than the manufacturer's recommended equivalent to the existing dose of MPH-IR.