NEW INSIGHTS INTO THE SCIENCE OF EMOTION UNRAVEL THE SEEMING NEUROLOGICAL MAGIC THAT TURNS EMOTIONS INTO SOCIAL EXPRESSIONS.
As Published in Seed Magazine
You’re at breakfast enjoying a mouthful of milk when it happens: the zygomatic muscles, anchored at each cheekbone, tug the corners of your mouth backwards and up. Orbicular muscles encircling your eyeballs slowly squeeze tight beneath wrinkling skin. A 310-millisecond-long noise explodes from your throat, extending to a frequency of 10,000 Hertz. Five shorter pulses of the “h” sound follow, five times per second, hovering around 6 Hertz, each lasting a fifteenth of a second. Your heart reaches 115 beats per minute. Blood vessels relax. Muscle tone softens. Abdominal muscles clench. The soft tissue lining your upper larynx vibrates 120 times per second as air blasts past. The milk spews forth. You are laughing.
May Lesser
Laughter, real laugh-till-you-cry laughter, is one of many human emotional expressions. Arguably, laughing and its tearful counterpart, crying, are the loudest, most intrusive non-linguistic expressions of our species. But for all of that familiarity, they are little-understood behavioral mysteries parading in the light of everyday experience. Though evolutionary biologists have long explored the mammalian origins of emotional expression, human laughs and cries only rarely become subjects of cognitive neuroscience. But that may not stay the case. Laughing and crying, being live demonstrations of emotion and its social expression, provide new entryways into the tangled pathways of the brain.
For centuries, philosophers and physiologists have puzzled over the phenomenon of emotion. Where are joy, sadness, fear located in the “gelatinous substance” of the brain? wondered nineteenth century phrenologist Franz Gall. How is emotion’s expression related to subjective feeling? In the 1890s, psychologists William James and Carl Lange suggested we don’t cry because we are sad, rather, “we feel sorry because we cry, angry because we strike, afraid because we tremble,” but other theories reigned. And though the James-Lange theory has had a resurgence in recent decades, not until fMRI technology revealed images of the emotional brain could we begin to empirically explore Shakespeare’s musing in
The Merchant of Venice: “Tell me where is fancy bred / Or in the heart, or in the head?”
A way of coming to a more integrated understanding of emotion is to surrender to the boundless accessibility of laughing and crying. I spent the last year occupied with such a task. The search for answers led me to areas as new to science as the mirror-neuron system, as painful as neurological disorders, and as artistic as method acting. There emerged a uniquely human science of emotion that begins to sew closed the doggedly dualistic notions of mind and body, heart and head.
A Ball of Emotion
“Try and keep your head still,” a soft voice murmured. “Just follow my fingers with your eyes.” The woman in the wheelchair couldn’t. At each attempted ascent, her eyes fell to center, unable to find visual anchor.
“How are you doing?”
“I’m fine,” she voiced over the course of eight seconds, her eyes calm and accepting. “I’m de-al-ing with i-t.” An array of wrinkles, right then, grew from her squinting eyelids. Rivulets of tears washed into the creases, bathing her cheeks in a Saran-wrap sheen. “Don’t mi-nd me,” she blurted.
Then, before anyone could reach out a hand in comfort, her jaw dropped and peals of laughter exploded into the boxy beige examination room at the Stanford University Neurology Clinic.
Dr. Josef Parvizi was unfazed. He sat on a short stool, his scarlet tie dangling as he leaned into her wheelchair, softly grasping her shoulder and stroking her hand. Parvizi, a neurologist at the Stanford School of Medicine, has a faint Iranian accent and an unwaveringly calm oval face. He’s seen patients like Nicole before.
Nicole’s crying started again, as though a memory had triggered a reaction that she would normally keep inside, like a filter between private thought and public expression was missing. Her sister, a rusty-haired woman clutching a leather bag, spoke for her. “So many things seem to upset her. There’s no rhyme or reason for an outburst,” she said. The doctor nodded. “It sounds like there are no brakes, like in a car. The brakes aren’t working so well for her emotion.” Her sister sighed in agreement. Nicole stopped rocking the wheelchair and tried once again to answer the doctors’ questions.
For the past 12 years, Nicole, 51, has lived with a progressing case of multiple sclerosis, a disorder in which her immune system attacks its own central nervous system, slowly nibbling away at the ability of her brain to send signals and coordinate muscle movements and cognition. Her MS has taken away her ability to walk and has limited her speech. Her disease now jeopardizes her ability to control her expressions of happiness and sadness. Today, Parvizi believes he will diagnose Nicole with a disorder called pathological laughing and crying, or PLC.
PLC develops after a brain injury, stroke, seizure, or, as with Nicole, during a neurodegenerative disorder. Usually, a lesion or tumor has encroached upon brain structures that govern emotional suppression and expression. It seems like the episodes of laughing or crying deploy without reason. Actually, it’s the result of lowered emotional thresholds. A passing funny thought that a healthy person could normally suppress, triggers laughter in Nicole. She experiences a rift between what she expresses and what she actually feels. Her laughter is a vast overestimation of her true feelings.
Cerebellar Vigilance
Parvizi asked Nicole to hold up her arm for a few seconds. Her raised arm shivered back and forth like a broken compass. The doctors looked at each other, recognizing the symptom. “Cerebellar ataxia,” Parvizi mouthed to another doctor. Cerebellar ataxia, a hallmark sign of multiple sclerosis, is the loss of muscle coordination. The cerebellum, a fist-sized 150-gram chunk of tissue, sits between the bottom of the brain and the top of the spinal cord. This structure accounts for 10 percent of the total volume of the brain, yet it contains half of all neurons. It coordinates the expression of involuntary, moment-to-moment muscle movements, fine-tuning motions we don’t need to think about to perform. When compromised by brain damage, the cerebellum, or “miniature brain” in Latin, can’t relay proper instructions to the brainstem, which executes many prepackaged muscle movements, including the diaphragm and facial contractions of laughing and crying.
Back in 2001 Parvizi was a graduate student at University of Iowa College of Medicine. He and his colleagues were studying a middle-aged landscaper who had suffered a stroke the year before and had been left with unexplained episodes of laughing and crying. A CAT scan presented damaged tissue in his cerebellum and brain stem, not surprising for a stroke victim. But the finding that the cerebellum could be a leading antagonist in the wrenching drama of PLC was something new—and perhaps game-changing—for emotional science.
The old explanation for PLC dates back to 1924, when neurologists worked with limited anatomical data. Basically, it was assumed that the healthy frontal lobe within the cerebral cortex usually regulates the emotional structures buried deeper in the brain. In that view, when those “higher” brain areas that endow us with rational, voluntary behavioral control fail, wild, pathological emotions are unleashed. But the voluntary pathway theory cannot explain why PLC patients often have no problem performing voluntary facial muscle movements. They can even mimic laughing and crying. Parvizi and his team knew that there had to be something going wrong with involuntary, automatic behavior patterns.
The seeming neurological magic through which an emotionally loaded stimulus turns into a physical expression is no simple process. But unlike the turn-of-the-century scientists, neuroscientists now know that it involves constant communication between networks. In neuroscience terms, major players are “induction sites” and “effector sites.” Induction sites, such as the amygdala or ventral striatum, pair a stimulus with an emotion. “You can think of an induction site like a switchboard deciding that when a snake comes, the best output is a sense of fear,” explains Parvizi. Effector sites, such as regions of the brainstem, execute the actual physical expression of that emotion, the part when we actually feel fear or joy. They are the warehouses producing the actual act of laughing or crying: moving the facial muscles up, spreading your lips, producing tears.
Induction and effector sites do not operate in a linear step-by-step fashion in a healthy brain. Instead, Parvizi’s research suggests, the cerebellum could be intercepting the induction signals before they reach the effector site, like a checkpoint. The “mini-brain” then makes sure our behavior plays appropriately in the social context, deploying a lifetime of cultural learning. It’s an idea that adds an entire new continent to the map of emotion: Rather than the brain’s frontal lobe serving as the geographic hotspot of rational decision making, instructions from the frontal lobe, along with autobiographical memories and tactile and visual data sent from other brain areas, wind up at the cerebellum. The cerebellum then adjusts the emotional response to match the social setting. Finally, the brainstem executes the response. Making sure that what would have been a shriek of laughter in the café is a soft giggle in a classroom is the cerebellum’s constant chore. But when this disciplinarian is ailing, as in some cases of PLC, behaviors can swing wild.
Parvizi’s PLC research has led him to believe that emotions, instead of being consciously controlled, are spontaneous reactions that rely on an intact involuntary brain system to be appropriately projected into the world. This distinction has major implications for our belief in self-control. Through cognitive neuroscience’s history, it’s been assumed that the brain’s evolutionarily newer frontal lobe regulates the more primitive regions of emotion, desire, and instinct, “as if there are beasts living in the basement, and the tower controls those beasts,” Parvizi says. He calls this an outdated Victorian-era bias that insists our free will should be able to conquer instinct. In fact, the brain’s structures are more interdependent. And those beasts of emotion are much, much more complex.
He says that we certainly can consciously control our expressions, even during those perilous mouthfuls of milk. We have both voluntary and involuntary systems, but it seems like the brain uses autopilot settings much more than conscious direction. “It’s an old notion that we regulate our behavior through a very conscious process, through a hierarchical top down process,” he says. “My idea is that we respond automatically in a context and that automatism is built partly from our culture.” In other words, early childhood socialization and lifetime experiences, coded into memories, factor into our automatic emotional responses. For example, in Japan, where emotional suppression is valued, people tend to avoid overt emotional displays. Parvizi acknowledges that this is an area wide open for debate. It is not yet clear, for instance, if those cultural pre-sets are stored in the cerebellum, or sent there from other brain areas.
The evaluation in the Stanford Neurology Clinic ended. Diagnosis: Pathological Laughing and Crying induced by Multiple Sclerosis. Nicole was wheeled out with a prescription for an antidepressant medication that will raise her brain’s emotional threshold and hopefully dampen her haphazard emotional outbursts. If the treatment works, it will take more than a passing sad memory to trigger her tears. The space where the Nicole sat was suddenly quiet. “And this is something we see over and over—,” Parvizi said, turning to me. “The problem isn’t a lack of voluntarism. It’s something much more.”
Acted Emotions
And then there are individuals who, unlike those patients with PLC, are so in control of emotional expression that they can willingly propel their bodies into the involuntary displays of laughing and crying. Intimate understanding of their own emotional physiology allows them to trigger or squelch emotional phenomena. As Hamlet puzzled, “Is it not monstrous that this player here, but in a fiction, in a dream of passion, could force his soul so to his own conceit, that from her working all his visage waned, tears in his eyes, distraction in his aspect, a broken voice, and his whole function suiting with forms to his own conceit?” The expression of genuine emotion without any personal reason to feel it is the prerogative of the performer, or the “player” in Shakespeare’s day. The talented performer spends hours refining and practicing the ability to laugh and cry in a matter of seconds in front of a sea of onlookers. For the actress, mastering the emotional is artistry; for the neuroscientist it is elusive science.
Josef Parvizi’s former professor back in Iowa was Antonio Damasio, who is now a neuroscientist at the University of Southern California. He has long been determined to understand how circumstances trigger emotions and how emotions then become feelings, as they do in actors and everyone else. He developed today’s leading theory of emotion, the somatic marker hypothesis, which builds on those of the giants before him, such as Carl Lange and William James, the scholars who first noted that feelings arose from perceptions of our body state. Of course, as Damasio’s more nuanced research methods have revealed, it is a bit more complicated than that.
To distinguish between human emotion and feeling, Damasio starts at the beginning. He sees emotion as a package of survival tools that originally evolved to help living beings navigate their environment safely, providing bodily warnings of dangerous situations. These responses later evolved to cause positive and negative feelings, which extended the impact of emotions by leaving a permanent stamp on memory. Over millions of years, this feedback process between organism and environment birthed foresight, and eventually, the human ability to respond to situations creatively.
Emotions familiar to us, such as happiness or anger, require an initial stimulus, a sight, smell, or memory. Physical changes follow. Feelings unfurl. Stimuli can even be simple actions. Back in 1992, Psychologist Paul Ekman found that voluntary smiles and grimaces produce changes in the autonomic nervous system. His study participants actually began to feel happy or sad or angry after following instructions to set their facial muscles in certain positions. “Psychologically unmotivated and ‘acted’ emotional expressions have the power to cause feeling,” Damasio writes. Enter the actress.
Once More, with Feeling
Credit: Jacques Gabay Donio
Sheila Donio first attempted to cry onstage as the character “Rizzo” in a stage production of Grease in 2001. She has acted since childhood and settled into professional acting career as a teenager in São Paulo, Brazil. “As I knew I wanted to cry on a specific scene,” she explained, “I started to work on Rizzo’s emotions at home, listening to the song used right before my crying scene. Studying Rizzo’s emotions with that specific soundtrack made my brain connect one thing with the other.” Method acting, techniques devised in the 1930s by Constantin Stanislavski, and later adapted by director Lee Strasberg, emphasize this use of sense memory. Students of this method learn to use personal memories of sensory details to trigger authentic physiological reactions.
Teaching herself, Sheila used this process to tap into the pathways of her brain responsible for the generation of crying. Crying on command became second nature. “Every time I heard that song, I would start to feel her anxieties and frustrations and the buttons for crying would show up in my body, ready to be pressed.” In fact, Sheila’s method of manipulating her body’s physiology is a living demonstration of Damasio’s theory of emotion.
In 2000, Damasio and his colleagues published the results of a landmark study in the field of emotion and feeling. The team asked 41 individuals to recall a particularly vivid emotional episode of their lives, memories charged with happiness, sadness, anger, or fear. (In a prior screening session, only the participants proven to experience emotional changes when recalling previous events were chosen.) Hooked up to a PET scanner, which detects specific activity in brain regions, the participants re-lived the chosen experience. As instructed, they each made a hand movement when they began to feel the anger, happiness, or sadness.
Electrodes measuring the volunteers’ physiological phenomena —things like heart rate and sweat levels in skin—registered drastic changes before the hands were raised. In other words, Damasio’s team found that people reported feeling emotional only after the eruption of a physical emotion. “It’s very important for you to think of emotion as an action, so crying is a component of emotion, never as a part of feeling. Feeling is a perception of the action we have,” he told me. Of course, only tears give Sheila confirmation that conjuring the emotionally tinted memory of Rizzo’s song, or “pushing her buttons for crying,” can trigger an authentic emotional cascade.
In that same study, Damasio found that the body-sensing region of the brain, the somatosensory cortex, came online as the feelings arose. Later, in 2006, he reported that for each basic emotion (e.g., happiness, sadness, anger, and fear) there is a distinct cardio-respiratory pattern. Linking these data sets together, in a technology-age tweaking of the James-Lange theory, Damasio suggests that feelings arise from “maps” continually forming in brain regions such as the somatosensory cortex. The brain doesn’t have simple “on” and “off “emotional switches. It is always in flux. Feelings are more than the brain’s perception of emotion; they are a constant process of mapping shifting body states.
Sheila makes daily use of those “maps.” “I study how my body reacts when I am crying for real, in real life. It’s all about breathing, for me. I get myself on the highway that leads me to cry. When I do improv theatre, this is how I find my emotions in 30 seconds,” she said. As Sheila adjusts her inhalations and exhalations, her somatosensory cortex detects the body map for crying. Genuine sadness follows the tears. The tears amplify the feelings, triggering sharper emotion, creating a positive feedback loop. What Sheila describes as a “highway,” Damasio thinks of more as a two-way traffic rotary.
‘E’-motion
Emotion in acting is not all about conjuring tears through physiological manipulations and memory recall. The audience in the back row needs to recognize the crying or joyous body just as intensely the people in the front row. That’s why the performer must play to the visual brain, or the mirrors reflecting within it.
Our brains can “mirror” the actions of those we watch. We feel our muscles clench when we watch a figure skater twist in the air, or when we crack a smile as a stage performer grins. That’s the work of the proposed “human mirror neuron network,” part of our visual brain. Basically, swaths of neurons in the human premotor cortex activate both when we are performing an action and watching someone else perform that action. The young science of our mirroring ability is rapidly gaining a spot in emotional neurobiology. After all, “motion” and “emotion” live just one letter apart.
In 1995, Vittorio Gallese of Parma University in Italy discovered mirror neurons in macaque monkeys. His continued explorations of mirroring behavior have most recently focused on the contagious nature of action and sound. He had a professional actor and actress perform sorrow and joy without uttering words—laughing and crying. He showed other participants silent versions of the actors’ embodiments and recorded the movement of their facial muscles. In a second condition, the participants heard only the sound of laughing or crying. “The results are pretty interesting,” he reported at a mirror neuron conference in 2007. “If you see someone laughing, you have strong activation of your zygomatic muscle, which is active when you laugh. If you see someone crying, you have an activation of the corrugator supercili. The same results are obtained with sound.” So, whether we hear laughing or crying, or watch the actions in silence, our smiling and frowning muscles automatically begin to respond. In essence, our emotions are contagious.
Sophie Scott, neuroscientist at University College of London, pressed ‘play’ on her iTunes and a cacophony of laughter and shrieks (as well as gagging and groans) attacked the air, causing both our faces to cringe and smile. In 2006, these were the sound samples used in a study into emotional mirroring. Twenty subjects listened to the samples, both positive and negative emotional vocalizations, while their brains were scanned with fMRI. They were told not to move their faces.
She was looking into the brain’s premotor cortex, a slice of which houses the neurons that control those facial expression muscles of smiling or laughing, the ones actors use so much. Her research team analyzed the participants’ brain activation while they heard the amused sounds. The disgust sounds were used as controls this time. Even though they were not actually smiling or laughing, the predicted slice of premotor cortex became active when the subjects heard the delight noises. These participants were experiencing other people’s apparent happiness through sound alone. In essence, their brains were starting to share a laugh.
This brings us back to Shakespeare’s cogent demand: ‘Tell me where fancy is bred/ Or in the heart, or in the head?’ Always immersed in theatre, he knew implicitly that authentic exuberance involved no forced smiles, but instead pink cheeks, watery eyes, and quickened breath. The evidence stood in front of him. Hundreds of years later, the technology of neuroscience provides a more complicated answer. Bodily emotion and moody feelings, head and heart, are constantly intertwined, reciprocal, looping processes. They do not exist separately. Once made visible, emotion’s expression requires some exacting architecture. This neurological machinery operates without permission, exposing our feelings to others. Still, to see how far fancy can travel outside the body, we’ve never needed fMRI scans. Just smile as you pass someone on the sidewalk and watch for the smile back.
Yet, she has been able to defy death. There is no better way to slip through a small loophole in the poorly drafted legislation of fatal brain disease than to have produced a lifetime’s worth of art. And my mother was an artist. She had been ever since she walked the halls of Massachusetts College of Art in the 1970s, so stunning she was likened to Greta Garbo, the Swedish actress who is listed as “the most beautiful woman that ever lived” in the 1954 edition of the Guinness Book of World Records. I’ve been told that a photography student followed her around with a camera.
