Mood Modulates Auditory Laterality of Hemodynamic Mismatch Responses during Dichotic Listening

Hemodynamic mismatch responses can be elicited by deviant stimuli in a sequence of standard stimuli even during cognitive demanding tasks. Emotional context is known to modulate lateralized processing. Right-hemispheric negative emotion processing may bias attention to the right and enhance processing of right-ear stimuli. The present study examined the influence of induced mood on lateralized pre-attentive auditory processing of dichotic stimuli using functional magnetic resonance imaging (fMRI). Faces expressing emotions (sad/happy/neutral) were presented in a blocked design while a dichotic oddball sequence with consonant-vowel (CV) syllables in an event-related design was simultaneously administered. Twenty healthy participants were instructed to feel the emotion perceived on the images and to ignore the syllables. Deviant sounds reliably activated bilateral auditory cortices and confirmed attention effects by modulation of visual activity. Sad mood induction activated visual, limbic and right prefrontal areas. A lateralization effect of emotion-attention interaction was reflected in a stronger response to right-ear deviants in the right auditory cortex during sad mood. This imbalance of resources may be a neurophysiological correlate of laterality in sad mood and depression. Conceivably, the compensatory right-hemispheric enhancement of resources elicits increased ipsilateral processing

Physicians' knowledge and continuing medical education regarding fitness to drive: a questionnaire-based survey in Southeast Switzerland

Valid information for physicians in Switzerland concerning knowledge and continuing education in traffic medicine is not available. Also, their attitude to the legally prescribed periodic driving fitness examinations is unclear. In order to gain more information about these topics, 635 resident physicians in Southeast Switzerland were sent a questionnaire (response rate 52%). In a self-estimation, 79% of the queried physicians claimed to know the minimal medical requirements for drivers which are important in their specialty. Statistically significant differences existed between the specialties, whereby general practitioners most frequently claimed to know the minimal medical requirements (90%). It appears that the minimal medical requirements for drivers are well known to the queried physicians. Fifty-two percent of the physicians favored an expansion of continuing education in traffic medicine. Such an expansion was desired to a lesser extent by physicians without knowledge of the minimal requirements (p < 0.001). A clear majority of the medical professionals adjudged the legally prescribed periodic driving fitness examinations as being an expedient means to identify unfit drivers. A national standardized form for reporting potentially unfit drivers to the licensing authorities was supported by 68% of the responding physicians. Such a form could simplify and standardize the reports to the licensing authorities

Role of ventral medullary catecholaminergic neurons for respiratory modulation of sympathetic outflow in rats

Sympathetic activity displays rhythmic oscillations generated by brainsteminspiratory and expiratory neurons. Amplification of these rhythmic respiratory-related oscillations is observed in rats under enhanced central respiratory drive or during development of neurogenic hypertension. Herein, we evaluated the involvement of ventral medullary sympatho-excitatory catecholaminergic C1 neurons, using inhibitory Drosophila allatostatin receptors, for the enhanced expiratory-related oscillations in sympathetic activity in rats submitted to chronic intermittent hypoxia (CIH) and following activation of both peripheral (hypoxia) and central chemoreceptors (hypercapnia). Pharmacogenetic inhibition of C1 neurons bilaterally resulted in reductions of their firing frequency and amplitude of inspiratory-related sympathetic activity in rats in normocapnia, hypercapnia or after CIH. In contrast, hypercapnia or hypoxia-induced enhanced expiratory-related sympathetic oscillations were unaffected by C1 neuronal inhibition. Inhibition of C1 neurons also resulted in a significant fall in arterial pressure and heart rate that was similar in magnitude between normotensive and CIH hypertensive rats, but basal arterial pressure in CIH rats remained higher compared to controls. C1 neurons play a key role in regulating inspiratory modulation of sympathetic activity and arterial pressure in both normotensive and CIH hypertensive rats, but they are not involved in the enhanced late-expiratory-related sympathetic activity triggered by activation of peripheral or central chemoreceptors