Anna Julia Karmann

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. OBJECTIVES To investigate this effect by examining the impact that variations in communicative relations (from being alone to being with an intimate other) have on the elements of the facial language used to communicate pain (types of facial responses), and on the degree of facial expressiveness. METHODS Facial responses of 126 healthy participants to phasic heat pain were assessed in three different social situations: alone, but aware of video recording; in the presence of an experimenter; and in the presence of an intimate other. Furthermore, pain catastrophizing and sex (of participant and experimenter) were considered as additional influences. RESULTS Whereas similar types of facial responses were elicited independent of the relationship between sender and observer, the degree of facial expressiveness varied significantly, with increased expressiveness occurring in the presence of the partner. Interestingly, being with an experimenter decreased facial expressiveness only in women. Pain catastrophizing and the sex of the experimenter exhibited no substantial influence on facial responses. CONCLUSION Variations in communicative relations had no effect on the elements of the facial pain language. The degree of facial expressiveness, however, was adapted to the relationship between sender and observer. Individuals suppressed their facial communication of pain toward unfamiliar persons, whereas they overtly displayed it in the presence of an intimate other. Furthermore, when confronted with an unfamiliar person, different situational demands appeared to apply for both sexes.

The role of inhibitory mechanisms in the regulation of facial expressiveness during pain

Although it is assumed that inhibitory control plays a role in regulating the degree of facial expressiveness, so far the specific type of inhibitory mechanism involved has not been identified. The present study was designed to investigate the association between different types of inhibitory mechanisms and the degree of facial expressiveness. Facial expressiveness during experimental pain was assessed using the Facial Action Coding System and facial electromyography (criterion variables). Different aspects of inhibitory functioning (Antisaccade task, Stroop task, questionnaire) were used as predictor variables. The degree of facial expressiveness was significantly predicted by the performance in the Antisaccade, but not the Stroop task or the questionnaire. The higher the ability was to inhibit saccadic eye movements, the lower was the degree of facial expressiveness. This data suggests that the degree of facial expressiveness is not regulated by inhibitory control in general, but specifically depends on inhibitory mechanisms regulating automatic motor responses.

[Sleep deprivation and pain: a review of the newest literature].

It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?ZusammenfassungEs ist mittlerweile unstrittig, dass Schlafentzug bzw. -fragmentierung zu Hyperalgesien führt, die sich nicht als allgemeine Veränderung der Somatosensorik erklären lassen. Welche Schlafphasen für die Deprivationswirkung am relevantesten sind, ist nicht ausreichend geklärt. Teilweise paradox anmutende Befunde zur Deprivationswirkung auf schmerzevozierte Hirnpotenziale einerseits und subjektives Schmerzerleben andererseits lassen komplizierte Veränderungen von Gating-Mechanismen vermuten. Da die Wirkungen auf Affekt und Schmerz dissoziieren können, ist ein gemeinsamer Wirkungsmechanismus unwahrscheinlich. Daten aus Tierstudien lassen vermuten, dass schlafentzugsbedingte Hyperalgesien bei bestehenden Neuropathien besonders ausgeprägt sind. Einige tierexperimentelle Ergebnisse sowie der Befund, dass Schlafdeprivation die endogene Schmerzhemmung [“conditioned pain modulation“ (CPM)] stört, führten zu der Annahme, dass das serotoninerge System die Wirkung von Schlafentzug auf das Schmerzsystem vermittelt. Andere Neurotransmitter und -modulatoren müssen aber weiterhin berücksichtigt werden. Klinisch gilt es zu klären, warum bei bestimmten Personen schlafentzugsbedingte Hyperalgesien besonders leicht auftreten und länger persistieren.AbstractIt has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?

Schlafentzug und Schmerz

It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?ZusammenfassungEs ist mittlerweile unstrittig, dass Schlafentzug bzw. -fragmentierung zu Hyperalgesien führt, die sich nicht als allgemeine Veränderung der Somatosensorik erklären lassen. Welche Schlafphasen für die Deprivationswirkung am relevantesten sind, ist nicht ausreichend geklärt. Teilweise paradox anmutende Befunde zur Deprivationswirkung auf schmerzevozierte Hirnpotenziale einerseits und subjektives Schmerzerleben andererseits lassen komplizierte Veränderungen von Gating-Mechanismen vermuten. Da die Wirkungen auf Affekt und Schmerz dissoziieren können, ist ein gemeinsamer Wirkungsmechanismus unwahrscheinlich. Daten aus Tierstudien lassen vermuten, dass schlafentzugsbedingte Hyperalgesien bei bestehenden Neuropathien besonders ausgeprägt sind. Einige tierexperimentelle Ergebnisse sowie der Befund, dass Schlafdeprivation die endogene Schmerzhemmung [“conditioned pain modulation“ (CPM)] stört, führten zu der Annahme, dass das serotoninerge System die Wirkung von Schlafentzug auf das Schmerzsystem vermittelt. Andere Neurotransmitter und -modulatoren müssen aber weiterhin berücksichtigt werden. Klinisch gilt es zu klären, warum bei bestimmten Personen schlafentzugsbedingte Hyperalgesien besonders leicht auftreten und länger persistieren.AbstractIt has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?

Associations of nocturnal sleep with experimental pain and pain catastrophizing in healthy volunteers

Strong alterations of night sleep (e.g., sleep deprivation, insomnia) have appeared to affect pain in inducing hyperalgesic changes. However, it has remained unclear whether everyday variations of night sleep in healthy individuals have any influence on pain processing. Forty healthy subjects were studied by portable polysomnography (PSG) and sleep questionnaire during two non-consecutive nights at home. Experimental pain parameters (pressure pain threshold, temporal summation = TS, conditioned pain modulation = CPM) and situational pain catastrophizing (Situational Catastrophizing Questionnaire = SCQ) were always assessed the evening before and the morning after sleep recording in a pain laboratory. Linear regression analyses were computed to test the prediction of overnight changes in pain by different sleep parameters. Significant prediction of changes in pain parameters by sleep parameters was limited (2 out of 12 analyses), indicating that everyday variations in sleep under non-pathological and low stress conditions are only weakly associated with pain.

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.

Schlafentzug und Schmerz@@@Sleep deprivation and pain: Ein Review der neuesten Literatur@@@A review of the newest literature

It has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?ZusammenfassungEs ist mittlerweile unstrittig, dass Schlafentzug bzw. -fragmentierung zu Hyperalgesien führt, die sich nicht als allgemeine Veränderung der Somatosensorik erklären lassen. Welche Schlafphasen für die Deprivationswirkung am relevantesten sind, ist nicht ausreichend geklärt. Teilweise paradox anmutende Befunde zur Deprivationswirkung auf schmerzevozierte Hirnpotenziale einerseits und subjektives Schmerzerleben andererseits lassen komplizierte Veränderungen von Gating-Mechanismen vermuten. Da die Wirkungen auf Affekt und Schmerz dissoziieren können, ist ein gemeinsamer Wirkungsmechanismus unwahrscheinlich. Daten aus Tierstudien lassen vermuten, dass schlafentzugsbedingte Hyperalgesien bei bestehenden Neuropathien besonders ausgeprägt sind. Einige tierexperimentelle Ergebnisse sowie der Befund, dass Schlafdeprivation die endogene Schmerzhemmung [“conditioned pain modulation“ (CPM)] stört, führten zu der Annahme, dass das serotoninerge System die Wirkung von Schlafentzug auf das Schmerzsystem vermittelt. Andere Neurotransmitter und -modulatoren müssen aber weiterhin berücksichtigt werden. Klinisch gilt es zu klären, warum bei bestimmten Personen schlafentzugsbedingte Hyperalgesien besonders leicht auftreten und länger persistieren.AbstractIt has now been established that sleep deprivation or fragmentation causes hyperalgesia which cannot be explained by a general change in somatosensory perception. However, it has not yet been clarified which of the sleep stages are most relevant for this effect. The seemingly paradoxical effects of sleep deprivation on pain-evoked brain potentials on the one hand and the subjective pain report on the other hand suggest complex changes in gating mechanisms. As the effects on pain and affect can be dissociated a common mechanism of action seems unlikely. Data from animal studies suggest that hyperalgesia due to sleep deprivation might be particularly strong under preexisting neuropathic conditions. Together with results from animal research the finding that endogenous pain modulation (CPM) is impaired by sleep deprivation suggests that the serotoninergic system mediates the effect of sleep deprivation on pain perception. However, other neurotransmitters and neuromodulators still have to be considered. The clinically relevant question arises why sleep deprivation induces hyperalgesia more easily in certain individuals than in others and why this effect then has a longer duration?