Psychosocial and neurobiological determinants of the inhibition of facial expressions of pain

Obwohl erste Befunde darauf hinweisen, dass Inhibitionsmechanismen bei der Regulation des mimischen Schmerzausdrucks eine wichtige Rolle spielen, kann dies bisher nicht als zuverlässige Schlussfolgerung gesehen werden. So ist zum jetzigen Zeitpunkt weder klar, welche Art von Inhibitionsmechanismus für die Regulation von Schmerzmimik besonders relevant ist, noch welche Gehirnareale an dessen Vermittlung ausschlaggebend beteiligt sind. Darüber hinaus ist bisher nicht bekannt, ob und wie die Inhibition des mimischen Schmerzausdrucks durch psychosoziale Faktoren beeinflusst wird. Im Rahmen der vorliegenden, publikationsbasierten Dissertation sollte daher geklärt werden, ob Inhibitionsmechanismen tatsächlich an der Regulation von Schmerzmimik beteiligt sind. Darüber hinaus sollte die Inhibition des mimischen Schmerzausdrucks bezüglich neurobiologischer sowie psychosozialer Aspekte genauer charakterisiert werden. Im Rahmen der ersten Studie konnte zunächst nachgewiesen werden, dass die Stärke des mimischen Schmerzausdrucks durch die Leistung in der Antisakkaden-Aufgabe (Indikator motorischer Inhibition) vorhergesagt werden kann. Dies war nicht der Fall, wenn die Leistung im Stroop-Test (Indikator von kognitiver und Verhaltensinhibition) oder der UPPS (selbst-berichtete Impulskontrolle) als Prädiktor verwendet wurden. Demnach scheint vor allem die Inhibition von automatisierten, motorischen Reaktionen bei der Regulation von Schmerzmimik eine Rolle zu spielen. Die zweite Studie befasste sich anschließend mit den neurobiologischen Grundlagen der Inhibition von Schmerzmimik. Hier konnte gezeigt werden, dass eine durch rTMS bedingte präfrontale Aktivitätsreduktion mit einer erhöhten Schmerzmimik einherging. Dies deutet darauf hin, dass präfrontale Aktivität maßgeblich an der Inhibition von Schmerzmimik beteiligt ist. In der letzten Studie wurde ermittelt, ob die Inhibition des mimischen Schmerzausdrucks bei Erwachsenen von psychosozialen Einflüssen – hier der Vertrautheit der Interaktionspartner – abhängt. Tatsächlich deuten die Daten an, dass die Inhibition von Schmerzmimik in Anwesenheit des Partners reduziert und im Beisein eines Versuchsleiters (zumindest bei Frauen) verstärkt wird. Die gewonnenen Erkenntnisse bestätigen demnach zunächst die Beteiligung von Inhibitionsmechanismen an der Regulation von Schmerzmimik und lassen zudem eine genauere Beschreibung des beteiligten Inhibitionsmechanismus und von dessen Einflussgrößen zu. Es scheint also – über ein „Inhibitionsgate“, das vornehmlich für die Inhibition automatischer, motorischer Reaktionen zuständig ist – zu einer „Ausgangskontrolle“ der automatisch generierten Mimikreaktion zu kommen. Dieses „Gate“ und somit das Ausmaß der Inhibition über die Schmerzmimik wird dabei von der Aktivität präfrontaler Areale reguliert, was schlussendlich die Stärke des mimischen Schmerzausdrucks (mit-)bestimmt. Die Aktivität dieses „Inhibitionssystems“ scheint dabei zudem immer vom Kontext beeinflusst zu sein, in dem sich die Person mit Schmerzen befindet. Je nach Vertrautheit der Interaktionspartner geben demnach erlernte soziale Regeln vor, wie stark die Inhibition von Schmerzmimik ausfallen soll

Facial expressions of pain: the role of the serotonergic system

Rationale Although interest in the neurobiology of facial communication of pain has increased over the last decades, little is known about which neurotransmitter systems might be involved in regulating facial expressions of pain. Objectives We aim to investigate whether the serotonergic system (5-HT), which has been implicated in various aspects of pain processing as well as in behavioral response inhibition, might play a role in facial expressions of pain. Using acute tryptophan depletion (ATD) to manipulate 5-HT function, we examined its effects on facial and subjective pain responses. Methods In a double-blind, placebo-controlled within-subject design, 27 participants received either an ATD or a control drink in two separate sessions. Approximately 5-h post-oral consumption, we assessed pain thresholds (heat, pressure) as well as facial and subjective responses to phasic heat pain. Moreover, situational pain catastrophizing and mood were assessed as affective state indicators. Results ATD neither influenced pain thresholds nor self-report ratings, nor catastrophizing or mood. Only facial responses were significantly affected by ATD. ATD led to a decrease in pain-indicative as well as in pain-non-indicative facial responses to painful heat, compared to the control condition. Conclusions Decrease in brain 5-HT synthesis via ATD significantly reduced facial responses to phasic heat pain; possibly due to (i) diminished disposition to display social behavior or due to (ii) decreased facilitation of excitatory inputs to the facial motor neuron

Relationship of 5-HTTLPR Polymorphism with Various Factors of Pain Processing:Subjective Experience, Motor Responsiveness and Catastrophizing

Although serotonin is known to play an important role in pain processing, the relationship between the polymorphism in 5-HTTLPR and pain processing is not well understood. To examine the relationship more comprehensively, various factors of pain processing having putative associations with 5-HT functioning were studied, namely the subjective pain experience (pain threshold, rating of experimental pain), catastrophizing about pain (Pain Catastrophizing Scale = PCS) and motor responsiveness (facial expression of pain). In 60 female and 67 male participants, heat pain stimuli were applied by a contact thermode to assess pain thresholds, supra-threshold ratings and a composite score of pain-relevant facial responses. Participants also completed the PCS and were grouped based on their 5-HTTLPR genotype (bi-allelic evaluation) into a group with s-allele carriers (ss, sl) and a second group without (ll). S-allele carriers proved to have lower pain thresholds and higher PCS scores. These two positive findings were unrelated to each other. No other difference between genotype groups became significant. In all analyses, "age" and "gender" were controlled for. In s-allele carriers the subjective pain experience and the tendency to catastrophize about pain was enhanced, suggesting that the s-allele might be a risk factor for the development and maintenance of pain. This risk factor seems to act via two independent routes, namely via the sensory processes of subjective pain experiences and via the booster effects of pain catastrophizing

Temporal Integration of Movement: The Time-Course of Motion Streaks Revealed by Masking

Temporal integration in the visual system causes fast-moving objects to leave oriented ‘motion streaks’ in their wake, which could be used to facilitate motion direction perception. Temporal integration is thought to occur over 100 ms in early cortex, although this has never been tested for motion streaks. Here we compare the ability of fast-moving (‘streaky’) and slow-moving fields of dots to mask briefly flashed gratings either parallel or orthogonal to the motion trajectory. Gratings were presented at various asynchronies relative to motion onset (from to ms) to sample the time-course of the accumulating streaks. Predictions were that masking would be strongest for the fast parallel condition, and would be weak at early asynchronies and strengthen over time as integration rendered the translating dots more streaky and grating-like. The asynchrony where the masking function reached a plateau would correspond to the temporal integration period. As expected, fast-moving dots caused greater masking of parallel gratings than orthogonal gratings, and slow motion produced only modest masking of either grating orientation. Masking strength in the fast, parallel condition increased with time and reached a plateau after 77 ms, providing an estimate of the temporal integration period for mechanisms encoding motion streaks. Interestingly, the greater masking by fast motion of parallel compared with orthogonal gratings first reached significance at 48 ms before motion onset, indicating an effect of backward masking by motion streaks

The influence of communicative relations on facial responses to pain: Does it matter who is watching?

BACKGROUND: Facial responses to pain are believed to be an act of communication and, as such, are likely to be affected by the relationship between sender and receiver

Temporal Integration of Movement: The Time-Course of Motion Streaks Revealed by Masking

Temporal integration in the visual system causes fast-moving objects to leave oriented ‘motion streaks’ in their wake, which could be used to facilitate motion direction perception. Temporal integration is thought to occur over ~100 ms in early cortex, although this has never been tested for motion streaks. Here we compare the ability of fast-moving (‘streaky’) and slow-moving fields of dots to mask briefly flashed gratings either parallel or orthogonal to the motion trajectory. Gratings were presented at various asynchronies relative to motion onset (from -200 to +700 ms) to sample the time-course of the accumulating streaks. Predictions were that masking would be strongest for the fast parallel condition, and would be weak at early asynchronies and strengthen over time as integration rendered the translating dots more streaky and grating-like. The asynchrony where the masking function reached a plateau would correspond to the temporal integration period. As expected, fast-moving dots caused greater masking of parallel gratings than orthogonal gratings, and slow motion produced only modest masking of either grating orientation. Masking strength in the fast, parallel condition increased with time and reached a plateau after 77 ms, providing an estimate of the temporal integration period for mechanisms encoding motion streaks. Interestingly, the greater masking by fast motion of parallel compared with orthogonal gratings first reached significance at 48 ms before motion onset, indicating an effect of backward masking by motion streaks