Imagine that your absolute rival sports team is in the league championship. In fact, they beat your own favorite team to do so. In the final minutes of the championship, though, your enemy team blows the game and […]

In my blog, I am intending to explore the neurological nature of theatrical performance. In the domain of Affective Neuroscience and Cognitive Psychology, it seems that the focus of most researchers stays on the processes involved in the genuine human emotional activity. Such activity as Acting, for example, involves mostly artificially stimulated emotions, and yet it requires full commitment and therefore its emotional processes are often labeled genuine, even though they are motivated by the need to perform. In real life, emotions are often uncontrolled. They are labeled as spontaneous, they don’t call before they show up at someone’s door, they just happen. In the Performing Arts, it is quite the opposite: emotions are provoked in performers, who then (ideally) receive reactions and empathy from the audience. I am interested in physical and psychological manifestations of artificially/purposefully stimulated emotive processing. I am hoping to demystify emotions using a scientific approach to the most ephemeral aspect of human behavior and nature. I am also exploring the concept of emotional prosody and the audial/musical/vocal basis of human emotions.

Human beings embody, express, process, inhibit, function, act, feel. All the verbs I just listed, along with many more, have as their sources the essential parts of what constitutes a human: body, mind, emotion, and behavior. In his dissertation, Kemp (2008) states that cognitive science acknowledges the central role of the body and enables a better understanding of understand the relationship between thought and expression (p. 20). Acting, on the other hand, does not explain the body-mind-soul relationship, but rather provides the richest material for exploration of and experimentation with human emotions. How does theatrical performance/activity conceptually relate to the cognitive science and affective neuroscience? The main things that both disciplines share is the idea of duality of the human nature. Are the emotions manifested through the body, or is the body producing emotions as integral parts of its purpose? Following the same logic, the acting traditions argue: can the physical work stimulate imagination to the point that the actor lives through the emotions of the character, or does the psychological approach to acting guarantee deep understanding and therefore meaningful expression? Kemp (2008) proposes that “the two approaches are in fact representative of positions on a continuum, rather than being mutually exclusive or necessarily oppositional. The empirically based concept of the embodied mind provides a foundation that explains the effectiveness of approaches to training and rehearsal that consciously link physicality and environment in the expression of meaning” (p . 24).

Unfortunately, until recently researchers and thinkers didn’t have a luxury to be inspired by scientific evidences of neurological activity and embodied cognition. And yet the juxtaposition of emotional and mental has always been present both in the science and the arts. Historically, acting has always been reflecting the latest trends in philosophical and cultural thought. For generations and even centuries, acting style maintained a very high level of artificiality, and what we know now as “believable acting” was simply a nonsense. In the early 19th century, just several decades before Psychology emerged, Henry Siddons and Johann Jacob Engel summarized the European pre-realistic modern acting style in their book “Practical Illustrations of Rhetorical Gesture and Action”. The book describes and illustrates several emotions and their physical expressions, in a way that is very similar to the system of discrete emotions used in Neuroscience. The pre-realistic school of acting assumed that “habit becomes a kind of nature” (p. 3). By providing illustrations of various gestures and poses each of which was connected to a specific emotion, the authors made sure that the conventional emotional expressions get institutionalized via theatre and therefore become internalized by many generations of theatre practitioners. Before there was a Psychology, acting relied on captured generalized emotional stereotypes.

One thing they were missing. Fake, artificial or not, emotions kept engaging the audiences by making them feel and empathize. As Lewis, Gibson and Lannon simply put it – Detecting an emotion changes the observer’s own emotional tone in the direction of the emotion he’s observing. (p.4) Some researchers of the 20th century would argue that theatre owed its glory to the mirror neurons.

Nearly 20 years ago mirror neurons were discovered in chimpanzees by Rizolatti and colleagues (Drenko, 2013, p. 26). After a series of tests, it was concluded that the mammalian brain is capable of engaging in what Lewis (2000) calls “the internal neural simulation of behavior it observes in others” (p.5). This theory clearly has a great potential to literally explain the functionality of performance in general and of theatre in particular. Since the beginning of the Western theatre tradition as we know it, the famous author of Poetics Aristotle described the main functions of Tragedy as Fear, Pity and Catharsis. While many historians argue whether those translations from Ancient Greek are accurate or even if Aristotle existed to begin with, there is not really much authentic evidence to work with since Greeks didn’t leave us their secrets on a flash drive. Assuming that this interpretation of Aristotle’s suggested dramatic functions is roughly compatible with the actual truth, we see how the list includes an affective state (fear/terror), empathy (pity) and purgation (catharsis).

Below is the full Aristotelian definition of tragedy: “Tragedy, then, is an imitation of an action that is serious, complete, and of a certain magnitude; in language embellished with each kind of artistic ornament, the several kinds being found in separate parts of the play; in the form of action, not of narrative; with incidents arousing pity and fear, wherewith to accomplish its katharsis of such emotions” (Butcher, S. H. (Ed.). (1917). The poetics of Aristotle. Macmillan)

Aristotle has been immortalized as the “Father” of Western Philosophy, Drama, and even of the Neuroscience. While his relation to the neuroscience may seem like a stretch, it worth mentioning that Aristotle was a trained doctor and researcher himself. While he acknowledged the duality of human nature manifested in tension between the mind and the heart, he did not believe in the brain’s involvement in emotions. (Gross, p. 247) If only he lived to see the mirror neurons, he would have known that empathy, essential component of Theatre, calls the brain its home. Empathy has been inscribed in the history of drama since the known beginning of it, as well as in the history of human kind. In the review article, Bernhardt and colleagues (2012) conclude that multiple studies, mostly based on empathy for pain, showed that “empathic responses recruit, to some extent, brain areas similar to those engaged during the corresponding first-person state” (p.). Linderberger (2010) describes the mirror neuronal process as two consecutive phases: stage one – imitation if the observed actions, second – internalization of the information and as a result the understanding of it (p.4). Those two stages may indeed constitute true empathy, and yet they only seem to be manifested in someone who is experiencing the event/emotion/story vicariously. When applied to the people impersonating and embodying characters in a story, the empathy cannot be enough.

Obviously, there is an endless number of acting techniques. The ones that prevail in the times contemporary with the modern neuroscience tend to be based on the psychological approach. Realistic acting is assumed to be the most common acting style people are exposed to, whether via television, cinema or live performances. We are going to set aside the improvisational methods and other non-traditional experimental approaches: in order to stay focused, let’s assume that generally realistic actors approach a character in a generally similar way. And this way involves two stages of processing. First, the actor gets acquainted with the character through reading his/her story. During this stage of the process, the actor is in the audience’s shoes: the incoming information resonates with his/her mind and perpetuates empathy. The actor’s goal is, however, not only to comprehend affectively the story and the character, but to undergo a process of transformation in order to portray/embody the given material. The actor must exist in the imaginary, or given circumstances: therefore, logically, his/her body needs to adjust and to start functioning as the one of the character. Since the body clearly includes the brain, can it be assumed that the actor rewires his/her brain to function as the one of the non-existing character, too? Kemp (2008) suggests that “the experience of emotion is something that is part of a disembodied consciousness rather than the processes of the body” (p.21). In this case, the emotions and the mind seem to be rather merged together, which contradicts the very traditional heart/mind dichotomy. But if we take a generalized realistic acting technique and trace every step of character’s coming to life, it appears that the consciousness and emotion walk hand in hand.

Once the actor internalizes the information about the character such as the background, demographics, looks, relationship history, beliefs, lifestyle (pretty much the equivalent of anyone’s first meeting with a psychologist), he/she connects the personal history and the given circumstances of the material that is being performed. Where is the line between the actor and the character? Where does the actor stop making decisions and begins choosing guided by emotions of his character? Creating a character is essentially reconstructing a human being from scratch, attributing all human aspects to his/her being/existence. Emotions then become the driving force of this process of creation. On stage or on screen, the actor creates a life, re-creates and re-tells a story. Without living emotions, the audience wouldn’t buy it (literally and figuratively).

More on current struggle to create an interdisciplinary bond between cognitive psychology and acting:

http://www.yale.edu/minddevlab/papers/GoldsteinBloomMindOnStageTiCS.pdf
References:

Bernhardt, B. C., & Singer, T. (2012). The neural basis of empathy. Annual review of neuroscience, 35, 1-23.

Butcher, S. H. (Ed.). (1917). The poetics of Aristotle. Macmillan.

Drinko, C. (2013). Theatrical improvisation, consciousness, and cognition. Palgrave Macmillan.

Engel, J. J., Siddons, H., & Engel, M. (1822). Practical Illustrations of Rhetorical Gesture and Action: Adapted from the English Drama: from a Work on the Subject by M. Engel.. Sherwood, Neely and Jones.

Gross, C. (1995). Aristotle on the Brain. The Neuroscientist, 1, 245-250.

Kemp, R. J. (2010). Embodied acting: cognitive foundations of performance (Doctoral dissertation, University of Pittsburgh).

Lewis, Gibson and Lannon. A primer on the neurobiology of inspiration. Published at http://www.terrypearce.com/pdf/PREREAD_gibson_et_al_061024.pdf

Lindenberger, H. (2010). Arts in the Brain; or, What Might Neuroscience Tell Us? Toward a Cognitive Theory of Narrative Acts, ed. Frederick Luis Aldama, Austin: University of Texas Press, pp. 13-35

Over the course of the next couple of months I plan to use these blog posts to explore topics dealing with how emotion influences the processes involved in person perception – the way we form impressions and make inferences about other people. In this inaugural post I want to delve into the processes guiding face perception as it relates to the perception of emotion.

Before we begin, I’ll take a moment to define a couple of terms that I use a lot when I talk about the sort of research that I like to talk about. These terms don’t necessarily carry the same definitions when we use them colloquially, so I think they bear some clarification. First, I talk a lot about social interactions (because that’s what I study!). In the context of empirical research, a social interaction describes the process of acting and reacting to people around us. An everyday example of a social interaction is two people having a conversation. When we try to study this sort of thing in the lab, we often need to isolate one or two very small aspects of the phenomenon we want to study. So we often operationalize aspects of a social interaction by defining the perceiver and the target. The perceiver is the person who is doing the looking or evaluating in a social interaction. The perceiver’s behavior in a social interaction happens in response to a target, which can be any sort of stimulus information about a person (e.g., a picture). Certainly, in real life the roles of perceiver and target are fluid in the context of an interaction—it depends on whose perspective you’re talking about. In the lab we tend to isolate one from the other so we can better understand the various processes underlying a given social interaction.

Ok, now that we have some common ground, let’s get to it.
Two paths: facial identity and facial expression
Back in 1986 Bruce and Young proposed a dual-systems model for face perception. Long story short, they suggested that when it comes to face perception, the perceiver uses two different routes for processing. Route 1 governs processing of information about facial identity, while route 2 governs processing of information about facial expression. About 15 years later Habxy and colleagues (2000) provided a compatible account of the neural substrates that underlie processes guiding face perception. By their account, system 1 governs static face information (for instance, face identity). These processes are implicated in similar brain regions, a major one being the fusiform gyrus (especially the fusiform face area [FFA]). On the other hand, system 2 governs changeable face information (for instance, facial expression). This sort of information tends to activate regions of the superior temporal sulcus (STS) in processing. We’ll keep these theories of how the brain processes face- and emotion-specific information and the underlying neural mechanisms in mind as we consider more recent research in the field of emotion and person perception.
Facial expression and memory for face identity
D’Argembeau and Van der Linden (2007) explored the influence of emotional face expressions on a perceiver’s automatic memory for the target’s face identity. Across two studies they explored whether perceivers would demonstrate superior memory when instructed to attend to a target’s emotional expressions (i.e., define the intensity of the expression), their personality trait (i.e., imagine a personality trait), or a specific structural feature of the face (i.e., indicate size of the nose). The results suggest that regardless of which aspects of a person’s face participants were instructed to attend to, they demonstrated better memory for face identities that expressed happiness compared to anger.

Overall, these results have some interesting implications for social interactions. First of all, they suggest that happy (compared to angry) faces are easier for a perceiver to process and subsequently remember. (So next time you want to make a lasting impression on a new acquaintance remember to smile ☺) This pattern may arise because when a face conveys anger, the perceiver’s attentional resources are averted to dealing with the potential threat in the environment. This could overwhelm a perceiver’s cognitive resources, preventing the perceivers from attending to and encoding the identity of the angry face.
Are there two separate systems?
These results put forth some evidence against the two-systems model for the perception of face identity and face expression. For instance, the finding that a target’s emotional expression could interfere with the processing and memory of the face suggests that the two systems may not be fully independent as originally suggested.

Indeed, recent work from den Stock and de Gelder (2014) provide compelling evidence against the theory of two independent systems. They presented participants with face/body compound stimuli and asked them to match the identity of the face in the original picture to two alternative choices. Participants demonstrated superior performance in the task when they were asked to match the identity of a neutral (compared to a happy or angry) face. Furthermore, performance was better for the emotional stimuli if the facial expression matched the bodily expression. These results demonstrate that task irrelevant emotional face and body expressions interfered with participants’ ability to process the identity of target faces. Thus, we find that perhaps the two systems originally posited for processing facial identity and facial expression may actually more intertwined than we once thought.

References
Bruce, V. & Young, A. W. Understanding face recognition. British Journal of Psychology. 77, 305–327 (1986).
Calder, A. J., & Young, A. W. (2005). Understanding the recognition of facial identity and facial expression. Nature Reviews. Neuroscience, 6(8), 641–51. doi:10.1038/nrn1724.
D’Argembeau, A., & Van der Linden, M. (2007). Facial expressions of emotion influence memory for facial identity in an automatic way. Emotion (Washington, D.C.), 7(3), 507–15. doi:10.1037/1528-3542.7.3.507.
den Stock, J. Van, & de Gelder, B. (2014). Face identity matching is influenced by emotions conveyed by face and body. Frontiers in Human Neuroscience, 8(February), 53. doi:10.3389/fnhum.2014.00053.
Haxby, J., Hoffman, E., & Gobbini, M. (2000). The distributed human neural system for face perception. Trends in Cognitive Sciences, 4(6), 223–233. doi:10.1016/S1364-6613(00)01482-0
 

Think of the last time you had to speak up in a large group of people you didn’t know well. Was it at a conference where you had to give a presentation to a room full of experts in your field? Was it when your teacher asked everyone to go around and say something interesting about themselves on the first day of class? Or was it when you tried to make a joke during your first dinner with your partner’s friends? In any case, you might remember feeling a bit anxious – that odd feeling in the pit of your stomach, your palms sweating, your heart racing.

Many individuals experience such mild anxiety in social situations, especially when it involves people they don’t know. Social anxiety disorder (SAD) is diagnosed only when this anxiety is so out of proportion to the actual situation that it becomes disabling to the person who is experiencing it. In fact, according to the DSM-5 (American Psychiatric Association, 2013), to be diagnosed with SAD, one must suffer “significant distress or impairment that interferes with his or her ordinary routine in social settings, at work or school, or during other everyday activities”. So if you pissed off your adviser because you didn’t even apply to speak at that conference, got a bad grade because you called in sick the first day of class even though attendance was required, or got broken up with because your partner had enough of your skipping events with her friends, and this level of anxiety has been typical for a while in your daily life, you might consider seeking some help.

You might also wonder, “Why do I feel this way? What is going on in my head?” Scientists in many disciplines such as clinical psychology, psychiatry, social psychology, cognitive psychology, and neuroscience have been trying to figure out exactly that for a while now. In this blog post, I will delve into this topic taking a neuroscientific approach and explore what scientists have discovered about what goes on in the brains of those with SAD.

The vast majority of studies conducted in this field investigate functional differences in the brains of those with SAD, compared to individuals without the disorder – the so-called “healthy controls” (HCs). In most of these studies, participants are shown stimuli relevant to social anxiety while scientists measure blood flow to certain areas of their brain as an indirect measure of brain activity. They often do this by using functional magnetic resonance imaging (fMRI) or positron emission tomography (PET). Investigating these activation patterns not only helps scientists understand the reasons behind the disorder, but it also helps them target certain processes for more successful treatment.

Many studies to date have shed light on this issue. In a recent fMRI study published in Biological Psychology, for example, Klumpp and colleagues (2012) had 29 generalized SAD (gSAD) patients and 26 HCs complete a modified Emotional Face Matching Task in which participants were shown a set of emotional faces and were asked to match a target face to the face in the set that expressed the same emotion. The researchers then compared activation in response to fearful (versus happy) faces between gSAD patients and HCs, and found more activation in the amygdala, insula, and the dorsal medial prefrontal cortex (DMPFC) of patients with gSAD.

Similar results have been found with different socially relevant stimuli as well. In another recent fMRI study published in Psychiatry Research, Blair and colleagues (2011) investigated the differences in brain function between those who had gSAD and HCs in response to self-referential comments. More specifically, the 15 participants with SAD and the 15 HCs were shown positive, neutral, or negative comments that were either from first-person viewpoints (e.g. “I am beautiful”) or second-person viewpoints (e.g. “You are beautiful”). Importantly, they were told that the comments were always about them, and that they just varied dependent upon whether they concerned another person’s point of view or their self-view. Interestingly, when they looked at the effects of simply hearing comments about the self, regardless of the point of view in which they were presented, they found more activation in the amygdala, DMPFC, and the lateral middle frontal cortex for those with SAD.

Using yet another different set of socially-relevant stimuli, and this time utilizing PET technology rather than fMRI, Tillfors and colleagues (2002) also examined the functional alterations in the brains of those with SAD. This time, instead of comparing patients with SAD to HCs, they compared the activation of brain areas within a group of 18 socially anxious individuals in two different experimental conditions. All participants were told that they would speak about a travel experience or vacation, both in front of an audience and alone. However, some participants spoke alone first (and thus anticipated the public speaking task), while others spoke in front of an audience first. Those in the anticipatory group indicated higher levels of anxiety as measured by heart rate and self-report. The results also indicated higher activation in the amygdaloid-hippocampal region, the dorsolateral prefrontal cortex, as well as the inferior temporal cortex as a function of anticipation of public speaking.

So, what do all these fancy names for brain parts mean? What is the take-home message here? Overall, these three studies, as well as others not cited here (see meta-analysis by Bruhl, Delsignore, Komossa, & Weidt, 2014), seem to converge on similar functional differences. Almost all relevant studies indicate an overactive amygdala, which is a region associated with arousal and negatively-valenced emotions. On the other hand, the prefrontal regions, which are often associated with emotion regulation, also seem active in most studies. Could it be possible that patients try to regulate their emotions by using prefrontal regions, but that this regulatory effect somehow does not reach the overactive amygdala (Bruhl et al., 2014)? Could it be that although patients are using their prefrontal cortex for emotion regulation, they are picking strategies such as emotional suppression that are unsuccessful at actually regulating their emotions, instead of picking more successful strategies such as reappraisal (Bruhl et al., 2014)? And beyond these questions about the basic neurobiology of SAD, what are some things that actually explain these differences? More on this soon.

References
[1] American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Arlington, VA: American Psychiatric Publishing.
[2] Blair, K. S., Geraci, M., Otero, M., Majestic, C., Odenheimer, S., Jacobs, M., et al. (2011). Atypical modulation of medial prefrontal cortex to self-referential comments in generalized social phobia. Psychiatry Research: Neuroimaging, 193, 38-45.
[3] Bruhl, A. B., Delsignore, A., Komossa, K., & Weidt, S. (2014). Neuroimaging in social anxiety disorder: A meta-analytic review resulting in a new neurofunctional model. Neuroscience and Biobehavioral Reviews, 47, 260-280.
[4] Klumpp, H., Andstadt, M., & Phan, K. L. (2012). Insula reactivity and connectivity to anterior cingulate cortex when processing threat in generalized social anxiety disorder. Biological Pschology, 89, 273-276.
[5] Tillfors, M., Furmark, T., Marteinsdottir, I., & Fredrikson, M. (2002). Cerebral blood flow during anticipation of public speaking in social phobia: A PET study. Biological Psychiatry, 52(11), 1113-1119.

Pictures
[Social anxiety comic]. Retrieved October 10, 2014, from: http://www.picturesinboxes.com/comics/2014-02-08-anxiety.jpg
[Prefrontal cortex and the amygdala]. Retrieved October 10, 2014, from: http://www.dana.org/uploadedImages/Images/Spotlight_Images/DanaGuide_CH14C31_P427_spot.jpg

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We are taught about our five senses from childhood: sight, smell, taste, touch, and hearing. Even from a young age, we know to “use our senses” to investigate the world around us. But these senses do more than just identify the world we live in, right? They must serve more functions than just being questions on a kindergarten worksheet or a short on a children’s TV show. Beyond our perception, our senses play an integral role in our emotional processing, learning, and interpretation. During various elements of emoting, our sensory cortices can be activated at different levels. In this blog series, I will explore how our different senses relate to our emotions (psychologically and neurologically). This specific blog post will examine how our senses relate to our emotional reactions, learning, and perception on a more general level.

Feeling happy yet? That’s a conceptual association!

Put simply, our emotional reactions can be guided by sensory information. Just because something looks gross, we may instinctively not like it. Thomson et. al (2010) defines this as a “conceptual association.” In other words, what we sense triggers a feeling. For me, coffee is linked with a sense of energy, positive feelings, and it being essentially a hug in a cup. These associations can be activated from me seeing a cup of coffee, smelling it, hearing a coffee maker, or tasting it. (Not so much by touch, I don’t really like sticking my hand in a cup of hot liquid!) Thomson et. al (2010) studied what emotional words were chosen to describe various chocolates. It was found that we associate different emotional words with different sensory qualities. Levels of bitterness, sweetness, creaminess, and even color impacted the participant’s emotional interpretation of what was all just chocolate. Deeper down, our sensory brain areas are involved with emotion too.

Our emotions and sensory cortices can impact one another in both directions. A review by Vuilleumier (2005) explained that emotions provide a boost to our sensory cortices. Neuroimaging showed that in response emotional, our sensory cortices have increased activation. Vuilleumier (2005) hypothesized that this is due to learning from the sensory characteristics of emotional situations. Think about if you heard a fire alarm or smelled smoke. These sensory cues mean it’s time to run (or walk safely to your nearest exit)! Similar findings were present in the research of fear memory. Using fear conditioning, Sacco and Sacchetti (2010) found that sensory cortices affect emotional memory. Rats were trained to associate visual, auditory, or olfactory cues with an aversive stimulus. When the respective secondary cortex was lesioned, the cues that were previously learned were lost. This means that there is some storage in the secondary sensory cortices when it comes to emotional memory.  Unless the ethical standards of human research change – and let’s hope they don’t – these findings can’t be replicated in humans. More research, perhaps with preexisting lesions or artificial ones from methods like TMS, would need to be done to see if we can generalize these findings.

As stated throughout this blog, our emotions and senses are very tightly intertwined. What we hear, see, taste, smell, and touch can provide us with information on how to feel. In the other direction, what we feel can be heavily influenced by what our senses are taking in. The next time you feel happy; know that something you’re sensing may have an impact in that euphoria. In the next blog, we’ll dive into how vision plays a role in our emotions.

 
References:
Sacco, T., & Sacchetti, B. (2010). Role of secondary sensory cortices in emotional memory storage and retrieval in rats. Science, 329(5992), 649-656. doi: 10.1126/science.1183165

Thomson, D. M., Crocker, C., & Marketo, C. G. (2010). Linking sensory characteristics to
emotions: An example using dark chocolate. Food quality and preference, 21(8), 1117-1125. doi: 10.1016/j.foodqual.2010.04.011

Vuilleumier, P. (2005). How brains beware: neural mechanisms of emotional attention. Trends in cognitive sciences, 9(12), 585-594. doi: 10.1016/j.tics.2005.10.011

[Coffee Cup Photograph] Retrieved October 9, 2014, from: http://www.shoplavazza.com