I first met Eduardo during my last year of neurology residency, in our aging and memory clinic. He was 56 years old and in robust physical health, having been an avid cyclist for much of his life. But he had a bookish side, too: He was an enthusiastic reader of history and led an informal book club that met monthly at his apartment. As a Dominican American, he was particularly interested in Latin American history and the New York City diaspora, and he often enlivened club meetings with his other passion: homemade Dominican specialties like pernil, bacalao, and pastelitos.

Over a period of eight months, however, all of these activities collapsed. Eduardo stopped playing tennis and cycling with his friends, instead preferring to lift weights almost obsessively in his building’s basement gym. Book club meetings became spaced further apart, and members began to leave because Eduardo made rude comments to them and sexual advances toward their wives. One night, Eduardo’s son came home to find the usually gastronomically picky Eduardo sitting on the sofa devouring an entire pint of supermarket ice cream.

It was time to see a neurologist.

What happened? Why did Eduardo rapidly drop out of life and abandon most of his activities? The reason became apparent once we assessed him at our clinic: Eduardo was suffering from frontotemporal dementia (FTD), a disease that causes progressive deterioration of the brain’s temporal lobes and orbitofrontal cortex. In Eduardo’s case, this was not entirely a surprise: His father and a paternal uncle had suffered from similar symptoms before their deaths but had not been formally diagnosed.

There are two traditional ways to think about brain-behavior relationships in FTD.

In the first model, the brain regions that were affected in Eduardo encode our knowledge of etiquette, social rules, or cultural practices. By destroying these regions, Eduardo’s FTD impaired his ability to follow these rules in everyday life. But this doesn’t actually capture the symptoms of Eduardo or other patients with FTD, as they are usually able to describe how they should act in these settings. Eduardo, for example, could report that his comments were rude when we repeated them to him, and he could discuss his prior cycling routes and various fine points of his recipes in detail. The knowledge was there; he just could not bring himself to act on it.

The second model, taught to generations of medical students and neurology residents, centers on motivation instead of knowledge. In this framework, FTD stems from disinhibition of “primitive” motivations like eating sweets or making sexual advances. This account draws on psychoanalysis and depth psychology, imagining the brain as composed of multiple strata with evolutionarily ancient layers driving these impulses and more recent ones “restraining” them. The psychiatrist Paul MacLean, for example, argued that our “reptilian” and “paleomammalian” brains provide our basic motivations and are inhibited by the “neomammalian” brain, which enables us to reason and use language. While normal humans can use their “neomammalian” brain to control their primitive motivations, injury to these higher regions allows these ancient strata to hijack our actions, causing behavior like Eduardo’s.

The problem with this account is that we have no neuroscientific evidence that these sorts of strata exist in the brain. Even the most “impulsive” behaviors involve complex coordination in distributed networks and are no less (neurally) purposeful and refined than “higher-level” abilities. For example, while Eduardo’s addiction to workouts and flippant, rude comments are socially inappropriate, they still require language and complex cultural skills, so it seems incongruous to say that they were ancient impulses waiting to be released.

In addition, his symptoms do not seem to arise solely from “disinhibition”; one could argue that his previous diverse interests were, in fact, overly inhibited. It was not just that he was devouring a pint of ice cream, but that he no longer spent hours making pernil for the Sunday feast.

The idea of higher and lower, inhibition and disinhibition, are in many ways remnants of older frameworks that we need to move beyond.

That being said, I think that this account is on the right track. Motivation is crucial, just not in the sense of primitive motivations controlled by higher-level intellectual or social abilities. Indeed, motivation is a fundamental feature of all behavior. While these neural systems may have ancient origins, in humans they form a highly evolved and encultured part of our nervous system.

The human difference is that we are particularly responsive to social motivations: We want to share positive experiences with others, and the mutual delight in doing so provides a major impetus for our everyday activities. Through many social interactions over time, those activities can themselves become motivating, generating an enormous array of seemingly “intrinsic” motivations like cycling, making pernil, or reading about Latin American history. Thus, our variety of motivations is not just an intrinsic product of our brains but results from the way the neural networks have been shaped by this shared enthusiasm over our lifetimes.

I think all of us can recognize this process. If you ask Eduardo or anyone why they participate in their favorite activities, they may initially say that they are intrinsically interesting or exciting. But if you push a little further, social history often emerges. It was a particular experience with family or friends that introduced someone to the career, sport, or hobby, and they gradually became drawn into it through interacting with others. Cycling, reading, and cooking only became motivating for Eduardo through a long history of interactions, whether with his family in the Dominican Republic or his friends in northern Manhattan.

[O]ur variety of motivations is not just an intrinsic product of our brains but results from the way the neural networks have been shaped by this shared enthusiasm over our lifetimes.

This suggests that the best way to describe Eduardo’s behavior is not “disinhibition” but a reduction in his socially generated diversity of motivations. Prior to his illness, Eduardo was motivated by a range of experiences, from the thrill of a grueling century ride on a road bike to the pleasures of discussing Latin American politics to the memories of home elicited by garlicky roast pork.

Afterward, his main rewards were sugary foods, solitary activities, and sex.

He was still motivated to act, but these motivations were directed into a few narrow channels rather than a wide variety of activities. The activities that were lost were those that depended on Eduardo’s long history of social interactions, and his FTD affected the crucial parts of the brain that enabled him to share motivations with others within complex social practices. Without these regions, he was left to pursue the most basic rewards.

But what actually forms these connections in humans? Whereas other animals can learn what fruits are delicious or which caves are safe from predators, these sorts of primary motivators cannot explain Eduardo’s cycling, book groups, or even his preference for pernil over ice cream.

Instead, what makes humans unique is our shared excitement in face-to-face interactions. Only through interactions with friends and family do these practices become rewarding in themselves. What Eduardo lost were the links between this sort of social motivation and the activities that became associated with it over the course of his life.