Face processing in adolescents with positive and negative threat bias.

BACKGROUND: Individuals with anxiety disorders exhibit a 'vigilance-avoidance' pattern of attention to threatening stimuli when threatening and neutral stimuli are presented simultaneously, a phenomenon referred to as 'threat bias'. Modifying threat bias through cognitive retraining during adolescence reduces symptoms of anxiety, and so elucidating neural mechanisms of threat bias during adolescence is of high importance. We explored neural mechanisms by testing whether threat bias in adolescents is associated with generalized or threat-specific differences in the neural processing of faces. METHOD: Subjects were categorized into those with (n = 25) and without (n = 27) threat avoidance based on a dot-probe task at average age 12.9 years. Threat avoidance in this cohort has previously been shown to index threat bias. Brain response to individually presented angry and neutral faces was assessed in a separate session using functional magnetic resonance imaging. RESULTS: Adolescents with threat avoidance exhibited lower activity for both angry and neutral faces relative to controls in several regions in the occipital, parietal, and temporal lobes involved in early visual and facial processing. Results generalized to happy, sad, and fearful faces. Adolescents with a prior history of depression and/or an anxiety disorder had lower activity for all faces in these same regions. A subset of results replicated in an independent dataset. CONCLUSIONS: Threat bias is associated with generalized, rather than threat-specific, differences in the neural processing of faces in adolescents. Findings may aid in the development of novel treatments for anxiety disorders that use attention training to modify threat bias.

Functional network dysfunction in anxiety and anxiety disorders.

A recent paradigm shift in systems neuroscience is the division of the human brain into functional networks. Functional networks are collections of brain regions with strongly correlated activity both at rest and during cognitive tasks, and each network is believed to implement a different aspect of cognition. We propose here that anxiety disorders and high trait anxiety are associated with a particular pattern of functional network dysfunction: increased functioning of the cingulo-opercular and ventral attention networks as well as decreased functioning of the fronto-parietal and default mode networks. This functional network model can be used to differentiate the pathology of anxiety disorders from other psychiatric illnesses such as major depression and provides targets for novel treatment strategies.

Independence of anticipatory signals for spatial attention from number of nontarget stimuli in the visual field.

Covertly attending to a location modulates the activity of visual areas even in the absence of visual stimulation. These effects are widespread, being found in the cortical representations of both attended and unattended portions of the visual field. It is not clear, however, whether preparatory modulations depend on subjects' expectation regarding the presence of additional nontarget stimuli in the visual field. Here, we asked subjects to endogenously direct attention to a peripheral location in the upper visual field, to identify the orientation of a low-contrast target stimulus, and we manipulated the number and behavioral relevance of other low-contrast nontarget stimuli in the visual field. Anticipatory (i.e., prestimulus) blood oxygenation level-dependent (BOLD) signal increments in visual cortex were strongest at the contralateral attended location, whereas signal decrements were strongest at the unattended mirror-opposite ipsilateral location/region of visual cortex. Importantly, these strong anticipatory decrements were not related to the presence/absence of nontarget low-contrast stimuli and did not correlate with either weaker target-evoked responses or worse performance. Second, the presence of other low-contrast stimuli in the visual field, even when potential targets, did not modify the anticipatory signal modulation either at target or nontarget locations. We conclude that the topography of spatial attention-related anticipatory BOLD signal modulation across visual cortex, specifically decrements at unattended locations, is mainly determined by processes at the cued location and not by the number or behavioral relevance of distant low-contrast nontarget stimuli elsewhere in the visual field.

Suprachiasmatic nucleus projection to the medial prefrontal cortex: a viral transneuronal tracing study.

The viral transneuronal labeling method was used to examine whether the suprachiasmatic nucleus (SCN) is linked by multisynaptic connections to the medial prefrontal cortex of the rat. In separate experiments, pseudorabies virus (PRV) was injected into one of the three different cytoarchitectonic regions that comprise the medial prefrontal cortex: infralimbic (Brodmann area 25), prelimbic (Brodmann area 32), and cingulate (Brodmann area 24) cortical areas. After 4-days survival, extensive SCN transneuronal labeling was found following infralimbic cortex (ILC) injections, but almost none occurred when the PRV injections were centered in the prelimbic or cingulate areas. In the ILC cases, transneuronal labeling was localized mainly in the dorsomedial SCN, although a moderate number of labeled neurons were found in the ventrolateral SCN. About 13% of the infected neurons were vasopressin immunoreactive and 4% were vasoactive intestinal polypeptide-positive. Another set of experiments was performed in which the paraventricular thalamic nucleus (PVT) was destroyed 2 weeks prior to making PRV injections into the ILC. Almost no SCN transneuronal labeling occurred in these animals, suggesting that the SCN projection to the ILC is dependent on a relay in the PVT. We propose that the SCN sends timing signals, via its relay in the PVT, to the ILC. This pathway may modulate higher-level brain functions, such as attention, mood, or working memory. Assuming that a homologous circuit exists in humans, we speculate that neurochemical changes affecting this pathway may account for some of the symptoms associated with clinical depression and attention-deficit/hyperactivity disorder.

The significance of carotid bruits in children: transmitted murmur or vascular origin, studies by pulsed Doppler ultrasound.

Forty-four youngsters with precordial murmurs and carotid bruits were evaluated clinically and independently, using pulsed Doppler ultrasound. The precordial murmur was evaluated with M-mode echocardiography combined with Doppler flow evaluation, and the carotid bruit was evaluated with peripheral vascular sector scan with Doppler flow evaluation. These ultrasonic techniques can identify abnormal blood flow at anatomic sites such as the aortic valve and in the carotid arteries. The patients had no symptoms and their condition, except for six, was mild enough that catheterization was not indicated. The clinical diagnosis of aortic stenosis was made in 30 children, and nine were thought to have no heart disease. On the basis of the ultrasonic examinations, 28 patients were diagnosed as having aortic stenosis and seven subjects had no intracardiac turbulence. However, there was disagreement in 14 instances; four of the six clinical "normals" were found to have aortic stenosis by pulsed Doppler echocardiography; six patients diagnosed as having mild aortic stenosis on a clinical basis were found to have no aortic abnormality. The results confirm that aortic stenosis usually presents as a murmur maximal in the aortic area, which is associated with a carotid bruit. Unfortunately, in at least one-fourth of the cases the murmur was not maximal at the aortic area, and a carotid bruit was found in several normal subjects. Since the consequences of over- or under-diagnosis of aortic stenosis are substantial, careful thought should be given to the differential diagnosis, and if possible, pulsed Doppler echocardiography should be utilized for a definitive statement of aortic valve-induced turbulence.