Effect of odor pleasantness on heat-induced pain: An fMRI study.

Odor modulates the experience of pain, but the neural basis of how the two sensory modalities, olfaction and pain, are linked in the central nervous system is far from clear. In this study, we investigated the mechanisms by which the brain modulates the pain experience under concurrent odorant stimulation. We conducted an fMRI study using a 2 × 3 factorial design, in which one of two temperatures (warm, hot) and one of three types of odors (pleasant, unpleasant, no odor) were presented simultaneously. "Hot" temperatures were individually determined as those perceived as painful (mean temperature = 46.9 °C). The non-painful "warm" temperature was set to 40 °C. Participants rated hot compared to warm stimuli as more intense and unpleasant, especially in the presence of an unpleasant odor. Parametric modeling on the intensity ratings activated the pain network, covering brain regions activated by the hot stimuli. The presence of an odor, irrespective of its valence, activated the amygdalae. In addition, the amygdalae showed stimulus-dependent functional couplings with the right supramarginal gyrus and with the left superior frontal gyrus. The coupling between the right amygdala and the left superior frontal gyrus was related to the intensity and unpleasantness ratings of the pain experience. Our results suggest that these functional connections may reflect the integrating process of the two sensory modalities, enabling olfactory influence on the pain experience.

Externalization Errors of Olfactory Source Monitoring in Healthy Controls-An fMRI Study.

Using a combined approach of functional magnetic resonance imaging (fMRI) and noninvasive brain stimulation (transcranial direct current stimulation [tDCS]), the present study investigated source memory and its link to mental imagery in the olfactory domain, as well as in the auditory domain. Source memory refers to the knowledge of the origin of mental experiences, differentiating events that have occurred and memories of imagined events. Because of a confusion between internally generated and externally perceived information, patients that are prone to hallucinations show decreased source memory accuracy; also, vivid mental imagery can lead to similar results in healthy controls. We tested source memory following cathodal tDCS stimulation using a mental imagery task, which required participants to perceive or imagine a set of the same olfactory and auditory stimuli during fMRI. The supplementary motor area (SMA) is involved in mental imagery across different modalities and potentially linked to source memory. Therefore, we attempted to modulate participants' SMA activation before entering the scanner using tDCS to influence source memory accuracy in healthy participants. Our results showed the same source memory accuracy between the olfactory and auditory modalities with no effects of stimulation. Finally, we found SMA's subregions differentially involved in olfactory and auditory imagery, with activation of dorsal SMA correlated with auditory source memory.

Some neuroanatomical insights to impulsive aggression in schizophrenia.

Patients with schizophrenia are at increased risk of engaging in violence towards others, compared to both the general population and most other patient groups. We have here explored the role of cortico-limbic impairments in schizophrenia, and have considered these brain regions specifically within the framework of a popular neuroanatomical model of impulsive aggression. In line with this model, evidence in patients with aggressive schizophrenia implicated structural deficits associated with impaired decision-making, emotional control and evaluation, and social information processing, especially in the orbitofrontal and ventrolateral prefrontal cortex. Given the pivotal role of the orbitofrontal and ventrolateral cortex in emotion control and evaluation, structural deficits may result in inappropriate use of socially relevant information and improper recognition of impulses that are in need for regulation. Furthermore, we have extended the original model and incorporated the striatum, important for the generation of aggressive impulses, as well as the hippocampus, a region critical for decision-making, into the model. Lastly, we discuss the question whether structural impairments are specific to aggressive schizophrenia. Our results suggest, that similar findings can be observed in other aggressive patient populations, making the observed impairments non-specific to aggressive schizophrenia. This points towards a shared condition, across pathologies, a potential common denominator being impulsive aggression.