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Abstract: Breathlessness is an aversive symptom in many prevalent somatic and psychiatric diseases and is usually experienced as highly threatening. It is strongly associated with negative affect, but the underlying neural processes remain poorly understood. Therefore, using fMRI, the present study examined the effects of breathlessness on the neural processing of affective visual stimuli within candidate brain areas including the amygdala, insula, and anterior cingulate cortex (ACC). During scanning, 42 healthy volunteers, mean (SD) age: 29.0 (6.0) years, 14 female, were presented with affective picture series of negative, neutral, and positive valence while experiencing either no breathlessness (baseline conditions) or resistive‐load induced breathlessness (breathlessness conditions). Respiratory measures and self‐reports suggested successful induction of breathlessness and affective experiences. Self‐reports of breathlessness intensity and unpleasantness were significantly higher during breathlessness conditions, mean (SD): 45.0 (16.6) and 32.3 (19.8), as compared to baseline conditions, mean (SD): 1.9 (3.0) and 2.9 (5.5). Compared to baseline conditions, stronger amygdala activations were observed during breathlessness conditions for both negative and positive affective picture series relative to neutral picture series, while no such effects were observed in insula and ACC. The present findings demonstrate that breathlessness amplifies amygdala responses during affective processing, suggesting an important role of the amygdala for mediating the interactions between breathlessness and affective states. [ABSTRACT FROM AUTHOR]

Abstract: Dyspnea is an aversive symptom in various diseases. High levels of negative affectivity are typically associated with increased dyspnea and changes in its neural processing. Recently, more dyspnea‐specific forms of negative affectivity such as dyspnea catastrophizing were suggested to contribute to increased perception of dyspnea beyond effects of rather unspecific negative affectivity such as general anxiety levels. The involved neural mechanisms have not yet been explored. Therefore, the present retrospective analysis examined the associations of dyspnea catastrophizing with neural activations during the anticipation and perception of dyspnea. Sixty‐six healthy volunteers underwent 20 blocks of inspiratory resistive load breathing with parallel acquisition of fMRI data. Loads inducing either severe or mild dyspnea (dyspnea conditions) were presented in alternating order, with each condition being visually cued (anticipation conditions). Dyspnea catastrophizing and general trait anxiety were measured with the Breathlessness Catastrophizing Scale (BCS) and the State‐Trait Anxiety Inventory, respectively. Correlating the BCS scores with neural activations during the perception of dyspnea yielded no significant results. However, during the anticipation of dyspnea, BCS scores correlated positively with activations of the anterior cingulate cortex (ACC), even after controlling for general anxiety levels. These activations in the ACC were not related to concurrent respiratory parameters. Results suggest that dyspnea catastrophizing in healthy volunteers is associated with stronger ACC recruitment during dyspnea anticipation. Given the established role of the ACC in processing affective states, affect regulation, and antinociception, this might reflect increased affective and/or top‐down modulatory processing in individuals with higher dyspnea catastrophizing when anticipating dyspnea. [ABSTRACT FROM AUTHOR]

Dyspnea anticipation and perception varies largely between individuals. To investigate whether genetic factors related to negative affect such as the 5-HTT LPR polymorphism impact this variability, we investigated healthy, 5-HTT LPR stratified volunteers using resistive load induced dyspnea together with fMRI. Alternating blocks of severe and mild dyspnea ('perception') were differentially cued ('anticipation') and followed by intensity and unpleasantness ratings. In addition, volunteers indicated their anticipatory fear during the anticipation periods. There were no genotype-based group differences concerning dyspnea intensity and unpleasantness or brain activation during perception of severe vs. mild dyspnea. However, in risk allele carriers, higher anticipatory fear was paralleled by stronger amygdala activation during anticipation of severe vs. mild dyspnea. These results suggest a role of the 5-HTT LPR genotype in fearful dyspnea anticipation. [ABSTRACT FROM AUTHOR]

The concept of cerebral plasticity suggests that the hand representation in somatosensory cortex is abnormal in congenital malformation disorders. To investigate this issue we studied 11 subjects with different degrees of upper extremity dysmelia due to thalidomide embryopathy in comparison to 10 control subjects. In the affected subjects fingers are typically missing in radio-ulnar order beginning with the thumb. Haemodynamic responses to electrical stimulation of the radial-most and ulnar-most fingers were measured in each subject using functional magnetic resonance tomography. The size of the hand area in the primary somatosensory cortex was estimated by calculating the Euclidian distance between corresponding activation peaks on the lateral postcentral gyrus. The cortical somatosensory hand representation was found to be significantly smaller in dysmelic subjects as compared with the control subjects (P < 0.001). The shrinkage of the hand area was not proportional to the number of missing fingers. Furthermore, the cortical representation of the ulnar fingers in the dysmelic subjects was shifted towards the cortical thumb representation of the control group. We suggest that the unproportional reduction of the hand area together with the observed shift may reflect use-dependent rather than malformation-induced reorganization of the somatosensory hand area. [ABSTRACT FROM AUTHOR]

Tactile object discrimination is one of the major manual skills of humans. While the exploring finger movements are not perceived explicitly, attention to the movement-evoked kinaesthetic information gates the tactile perception of object form. Using event-related functional magnetic resonance imaging in seven healthy subjects we found one area in the right superior parietal cortex, which was specifically activated by kinaesthetic attention during tactile object discrimination. Another area with similar location in the left hemisphere was related to the maintenance of tactile information for subsequent object discrimination. We conclude that kinaesthetic information is processed in the anterior portion of the superior parietal cortex (aSPL) with a right hemispheric predominance for discrimination and a left hemispheric predominance for information maintenance. [ABSTRACT FROM AUTHOR]

ABSTRACT The authors investigated a 38-year-old patient with focal cortical dysplasia in the right precentral cortex using positron emission tomography and functional magnetic resonance imaging to localize the hand and finger motor representations. The patient presented clinically with epilepsia partialis continua, supposed to originate from the perirolandic area harboring the cortical malformation. Both methods revealed an abnormal bilateral activation of motor cortex during left-hand finger movements. The results suggest that the so-called eloquent but nevertheless pathological dysplastic cortex accommodates motor representations. [ABSTRACT FROM AUTHOR]

AbstractIn the magnocellular nuclei of the hypothalamus, there is a rich vascular network for which the function remains to be established. In the supraoptic nucleus, the high vascular density may be one element, which together with the water channel aquaporin-4 expressed in the astrocytes, is related to a role in osmoreception. We tested the osmoreception hypothesis by studying the correlation between vascular and cellular densities in the paraventricular nucleus and the supraoptic nucleus. Whether aquaporin-4 is likely to contribute to osmoreception was tested by studying the distribution in the magnocellular nuclei of the hypothalamus. The high vascular density may also reflect a high metabolic activity due to the synthesis of vasopressin and oxytocin. This metabolic hypothesis was tested by studying the regional cytochrome oxidase histochemistry, the local cerebral blood flow, and the density of glucose transporter type-1 in the supraoptic and paraventricular nuclei. All the magnocellular nuclei were characterized by an extended and intense aquaporin-4 labelling and a weak cytochrome oxidase histochemistry. The highest vascular density was found in the supraoptic nucleus and the magnocellular regions of the paraventricular nucleus. The local cerebral blood flow rates were surprisingly low in the paraventricular nucleus and the supraoptic nucleus in comparison to the cerebral cortex. Furthermore in these nuclei, the antibody for glucose transporter type-1 revealed two populations of vessels differing by their labelling intensity. The similarities observed between the different nuclei suggest that, in the hypothalamus, all magnocellular regions sense the plasma osmolarity. The low local cerebral blood flow, and the patterns of glucose transporter type-1 labelling and cytochrome oxidase histochemistry suggest that the high vascularization of these hypothalamic nuclei is not related to a high metabolic capacity in basal conditions. [ABSTRACT FROM AUTHOR]

There is substantial evidence for an important modulating role of monoamines (catecholamines and serotonin, 5-HT) in the rostral ventral medulla (RVM), a region which plays an important role in cardiovascular and nociceptive functions. We investigated in slices the role of endogenous monoamines in the synaptic control of the activity of rat RVM neuronal populations using intracellular recordings in the lateral RVM plus lateral aspect of nucleus paragigantocellularis lateralis. A triple-labelling protocol allowed us to identify the location of impaled neurons and their eventual monoaminergic phenotype within the serotonergic and catecholaminergic populations of the RVM. Focal electrical stimulation revealed the existence of a functional monoaminergic input onto RVM neurons which was mediated by endogenous 5-HT acting at inhibitory 5-HT1A receptors but did not involve noradrenergic neurotransmission. The slow 5-HT-mediated inhibitory postsynaptic potential (IPSP) was only observed in the regularly discharging neurons, which were found to be neither catecholaminergic nor serotonergic. The synaptic release of 5-HT was, itself, under an inhibitory control involving GABAA (gamma-aminobutyric acid) receptors. Moreover, we characterized the effect of the 5-HT-releasing agent fenfluramine on this functional 5-HT-mediated synaptic transmission. Our results show that the effect of fenfluramine is biphasic consisting of an initial prolongation of the serotonergic IPSP followed by a decrease in amplitude. Our data provide a basis for the previously reported inhibitory effects of exogenously applied serotonin agonists/antagonists on the autonomic functions controlled by the RVM. This 5-HT pathway, which functionally links the serotonergic and catecholaminergic regions, might play an important role in cardiovascular and nociceptive functions.