Emotion’s Alchemy

Feature / by Genevieve Wanucha /

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

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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.

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.

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