Mapping expectancy-based appetitive placebo effects onto the brain in women.

Suggestions about hunger can generate placebo effects on hunger experiences. But, the underlying neurocognitive mechanisms are unknown. Here, we show in 255 women that hunger expectancies, induced by suggestion-based placebo interventions, determine hunger sensations and economic food choices. Functional magnetic resonance imaging in a subgroup (n = 57/255) provides evidence that the strength of expecting the placebo to decrease hunger moderates medial prefrontal cortex activation at the time of food choice and attenuates ventromedial prefrontal cortex (vmPFC) responses to food value. Dorsolateral prefrontal cortex activation linked to interference resolution formally mediates the suggestion-based placebo effects on hunger. A drift-diffusion model characterizes this effect by showing that the hunger suggestions bias participants' food choices and how much they weigh tastiness against the healthiness of food, which further moderates vmPFC-dlPFC psychophysiological interactions when participants expect decreased hunger. Thus, suggestion-induced beliefs about hunger shape hunger addressing economic choices through cognitive regulation of value computation within the prefrontal cortex.

Late-Onset OCD as a Potential Harbinger of Dementia With Lewy Bodies: A Report of Two Cases.

OBJECTIVES: Obsessive-compulsive disorder usually begins in adolescence or young adulthood. OCD cases appearing after the age of 50 years are rare, most often associated with inflammatory, brain lesions, or neurodegenerative comorbidities. We describe two cases of late-onset obsessive compulsive disorder followed by the development of Dementia with Lewy Bodies and review the links between these two disorders. METHODS AND RESULTS: We describe the clinical history of two patients that first showed OCD symptoms at an atypical age (>60 years). After several failed treatment attempts, they were hospitalized in our unit. Both presented severe sensitivity to antipsychotic agents that led to a diagnosis of Dementia with Lewy Bodies. Administration of cholinesterase inhibitors was associated with decrease of psychiatric symptoms in both cases. In addition to those clinical observations, a systematic review of the literature suggests that, beyond prefrontal cortex, temporal lobe and putamen have important roles in OCD pathophysiology. Based on these findings, we discuss four hypotheses to explain the sequential appearance of OCD and DLB symptoms. First, we considered the possibility that comorbidity of OCD with DLB was coincidental. Second, we propose to interpret OCD symptoms as motor stereotypies. Third, we hypothesize that late-onset OCD might be a symptom of late-onset depression. Four, we hypothesize that through early deterioration of basal ganglia, DLB caused the onset of OCD. CONCLUSION: In conclusion, we recommend that cases of late-onset treatment-resistant OCD should be carefully tested for possible organic etiologies, and for DLB in particular.