Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
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mise à jour du
26 mai 2013
PNAS
2012;109(48):
19816-19821
Neural basis of contagious itch and
why some people are more prone to it
 
Henning Holle, Kimberley Warneb, Anil K. Seth,
Hugo D. Critchley, Jamie Ward
 
Department of Psychology, University of Hull, United Kingdom  
 

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 Tous les articles sur la contagion du bâillement
All articles about contagious yawning
 
 
Abtsract: Watching someone scratch himself can induce feelings of itchiness in the perceiver. This provides a unique opportunity to characterize the neural basis of subjective experiences of itch, independent of changes in peripheral inputs. In this study, we first established that the social contagion of itch is essentially a normative response (experienced by most people), and that the degree of contagion is related to trait differences in neuroticism (i.e., the tendency to experience negative emotions), but not to empathy. Watching video clips of someone scratching (relative to control videos of tapping) activated, as indicated by functional neuroimaging, many of the neural regions linked to the physical perception of itch, including anterior insular, primary somatosensory, and prefrontal (BA44) and premotor cortices. Moreover, activity in the left BA44, BA6, and primary somatosensory cortex was correlated with subjective ratings of itchiness, and the responsivity of the left BA44 reflected individual differences in neuroticism. Our findings highlight the central neural generation of the subjective experience of somatosensory perception in the absence of somatosensory stimulation. We speculate that the habitual activation of this central "itch matrix" may give rise to psychogenic itch disorders.

Ward J, Burckhardt V, Holle H. Contagious scratching: shared feelings but not shared body locations. Front Hum Neurosci. 2013
 
C. Schut, S. Grossman, U. Gieler, J. Kupfer, G. Yosipovitch. Contagious itch: what we know and what we would like to know. Front Hum Neurosci. 2015; 9: 57.
 
Itch is to some degree socially contagious. Subjective feelings of itchiness and observable increases in scratching can be evoked by watching someone scratch himself or by listening to a lecture on dermatologic conditions (1, 2). Although many aspects of the neurobiology of itch are now appreciated (3, 4), the standard definition of itch ("an unpleasant sensation associated with an urge to scratch") and its description as a symptom within clinical disorders remain essentially subjective and based on self-report. The study of the neural basis of contagious itch presents a unique opportunity to explore the neural basis of subjective itch experience that is dissociated from the normal peripheral inputs.
 
Functional neuroimaging investigations of itch [predominantly functional MRI (fMRI)] typically use an invasive, localized administration of histamine to induce itch (5&endash;8). This approach has revealed the engagement of a network of regions (the so-called "itch matrix") that includes the anterior insula, cingulate cortex, primary somatosensory cortex, premotor cortex, prefrontal cortex, thalamus, and cerebellum. Within this network, there is functional specialization that reflects the multifaceted nature of itch (i.e., its sensory, motor, and affective attributes), with the proposal that anterior insula and cingulate cortex may code the affective components of itch (4). Of note, these regions are also linked to the processing of (and awareness of) interoceptive bodily signals, including pain, cardiovascular activity, and hunger (9, 10). These internal signals are motivationally salient, and thus their representation may correspondingly engender an urge for action (11)&emdash;that is, scratching in the case of itch.
 
The planning of scratching movements is linked to premotor activity, whereas the intention to scratch (or not) is linked to engagement of the prefrontal cortex (12), consistent with this area's recognized role in willed actions (13). Primary and secondary somatosensory cortices have been proposed to support the sensory (i.e., spatial, temporal, and intensity) aspects of the experience (4); however, activity within almost all parts of the itch matrix is correlated with subjective ratings of itch intensity (5, 6, 14), suggesting interdependence of the sensory, motor, and affective components of itch. Previous fMRI studies were constrained by the methodological limitation that the experience of histamine-induced itch emerges rather slowly, taking approximately 1 min to reach peak intensity after onset of infusion (5), followed by a slow decay.
 
This time course means that little of the moment-to-moment fluctuation in subjective itchiness can be related to evoked changes in brain activity, constraining analytic power. We show that visual induction of itch does not suffer from this limitation. Although no previous study has examined the neural correlates of visually induced itch, several researchers have suggested that the "mirror neuron system" may be essential for contagious itching (2, 4).Mirror neurons, first reported in the macaque brain, respond to both a self-executed action and the sight of an action performed by another person (15). In macaques, mirror neuron-containing regions include the premotor and inferior frontal cortices and inferior parietal lobe (16). Neurons with similar properties have been observed in the human brain as well (17). In humans, this system may extend beyond action perception to perception of feeling states. For instance, Carr et al. (18) suggested that viewing a facial expression activates emotion-related parts of the brain via the motor-based mirror system, and that this could be the neural basis of empathy (19). There is compelling evidence linking empathy with some forms of emotional or behavioral "contagion" (20, 21), although contagious itch has not been considered in any previous studies. However, some studies did not implicate actionbased mirror systems as the interface between perception and feeling (22, 23), but suggested instead that feeling states can be shared without obligatory motor simulation.
 
itch
 
 
Discussion
 
The first important finding of the present study is that on a behavioral level, social contagion of itch is a normative response (i.e., experienced by most people). When participants were free to scratch, most (64%) did so at least once. This puts itch on a par with other types of socially contagious behavior, including laughter (47%; ref. 27) and yawning (40&endash;60%; refs. 21, 28). Furthermore, participants who experienced stronger feelings of itchiness during the experiment also tended to spontaneously scratch themselves more often when free to do so, indicating a correspondence between self-report and observable behavior. Our findings characterize the central neural substrates mediating the social contagion of itch by identifying regions that support the subjective experience of itch. Importantly, observing itch activated the same set of brain regions associated with feelings of itch induced by an irritant, such as histamine (5&endash;7). This shared network includes the anterior insula, premotor cortex, primary somatosensory cortex, and prefrontal cortex. One region not activated in our study but typically activated by chemical induction of itch is the midcingulate cortex, although not all studies of itch have reported activity here (14, 29). The magnitude of activation across this "itch matrix" reflects the main effect of viewing itch-related videos (relative to non-itch control stimuli), and tends to correlate with the subjective intensity of itchiness reported for these stimuli.
 
There is good evidence that the anterior insula is a core node in the network for shared pain (reviewed in ref. 23), and our results demonstrate that itch may be shared in the anterior insula as well. Furthermore, the response in the right anterior insula was sustained throughout the duration of the stimulus, in contrast to most other regions, which displayed a strong response in the early phase only. The (right) anterior insula is part of a tightly connected neural network engaged in interoceptive awareness (30), that is, representation of motivationally salient subjective feelings related to the body's internal state, including C-fiber&endash;mediated sensations such as itch, tickle, and visceral pain (31). These insular bodily representations may subserve at least two functions relevant to contagious itch. First, the anterior insula may act as a comparator in a predictive coding model of interoception, according to which subjective feeling states arise from top-down predictions of interoceptive signals (32). Second, these predictive representations may allow simulation of how a specific stimulus feels to others (33). Combining these views, anterior insula activity thus may be related to sharing the unpleasant bodily sensations that accompany itch.
 
Several of the brain regions linked to contagious itch are implicated in the simulation of actions (mirror systems), including the premotor cortex (BA6) and adjacent BA44 (34, 35). The primary somatosensory cortex (BA2) is also commonly activated during action observation (34), but also plausibly could code the sensory aspects of itch. In all three of these regions, activity was greatest in the earlier half of the stimulus presentation. This is more consistent with involvement of these regions in the perception of itch than in, say, the generation of scratching urges. The latter would be expected to build up over the duration of the stimulus (although we did not explicitly measure how the subjective experience unfolds over time). However, each of these regions likely has a relatively different functional contribution that remains to be fully elucidated. The area of activity in primary somatosensory cortex lies in the left hemisphere hand area (36), suggesting that it may code the sensory effects of scratching (rather than the location being scratched). Along with a role in the simulation of actions, the premotor cortex also responds to somatosensory stimuli (37&endash;39) and the sight of touch (40&endash;42); thus, in principle, its role also may be sensory-based rather than action-based. However, premotor and somatosensory cortices differ in the degree to which they are also activated by the control condition of tapping. The premotor region does not respond to this control action relative to fixation, whereas somatosensory cortex does respond.
 
This could reflect different motoric demands that affect primarily the premotor cortex; for example, scratching requires complex manipulation of fingers, but tapping is a far simpler wrist-based action. Itch-related activity in the left BA44 is correlated with neuroticism, and neuroticism itself has been identified as the sole reliable trait predictor of individual differences in subjective feelings of itch contagion. This trait is known to exacerbate certain clinical symptoms, such as chronic pain (43), and is a predisposing influence in various psychopathologies (44). The importance of neuroticism as opposed to empathy might reflect a key difference between the social processing of itch versus pain that may originate in distinct motivational biases toward social proximity (pain) or distance (itch). The prefrontal cortex is generally implicated in the control of cognition and behavior, and in the present context it may serve a gating (attention-related) function that modulates the degree of contagion. Finally, some patients report persistent itch sensations (often accompanied by a belief of infestation) but appear dermatologically normal (45). It is likely that the same central mechanisms responsible for itch sensations induced by observing itch in others (an essentially normative response) is responsible for itch induced by self-generated thoughts of itching or infestation (which may become established as dominant overvalued representations in a minority of persons). Individual differences within this network, also related to personality traits, may modulate the extent to which this contagion is triggered by environmental cues versus occurring spontaneously and habitually (46, 47). Further research is warranted to explore the link between contagious itching and compulsive itching.