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emotionalchemy inline
physics.subha.peperonity.net

neurological magic that turns emotions into social

New insights into the science of emotion unravel the seeming neurological magic that turns emotions into social expressions.

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.

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 Nicole1 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 feeling.

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.

Laughing and crying provide new entryways into the tangled pathways of the brain.

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. ...
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