We start with the case of a woman who experienced unbearable tragedy. In 1899, this Parisian bride, Madame M., had her first child. Shockingly, the child was abducted and substituted with a different infant, who soon died. She then had twin girls. One grew into healthy adulthood, while the other, again, was abducted, once more replaced with a different, dying infant. She then had twin boys. One was abducted, while the other was fatally poisoned.
Madame M. searched for her abducted babies; apparently, she was not the only victim of this nightmarish trauma, as she often heard the cries of large groups of abducted children rising from the cellars of Paris.
As if all this pain was not enough, Madame M.’s sole surviving child was abducted and replaced with an imposter of identical appearance. And soon the same fate befell Madame M.’s husband. The poor woman spent days searching for her abducted loved ones, attempting to free groups of other abducted children from hiding places, and starting the paperwork to divorce the man who had replaced her husband.
. Illustration Jackie Ferrentino
In 1918, Madame M. summoned the police to aid her in rescuing a group of children locked in her basement. Soon she was speaking with a psychiatrist. She told him she was the direct descendant of Louis XVIII, the queen of the Indies, and of the Duke of Salandra. She had a fortune of somewhere between 200 million and 125 billion francs, and had been substituted as a toddler in a conspiracy to deny her this money. She was constantly under surveillance, and most, if not all, of the people she encountered were substituted doubles, or even doubles of the doubles.
The psychiatrist, Joseph Capgras, listened patiently. It’s delusional psychosis—disordered thought, grandiosity, paranoia—he thought. Pretty standard fare. But then again, no one had ever described the particular delusion of a loved one being replaced by an identical double. What could that be about?
You insist you’ve never seen this person before, but your brain circuitry knows exactly who it is.
Later, describing Madame M. in a case report, Capgras and his intern Jean Reboul-Lachaux wrote, “The feeling of strangeness develops in her, and it jostles with the feeling of familiarity that is inherent in all recognition. But it does not totally invade her consciousness; it does not distort either her perceptions or her memory images.” To Capgras, this was extraordinary. Recognition and familiarity elicited different emotions in Madame M. Her problem was she couldn’t reconcile the two emotions. The delusion of doubles wasn’t a sensory delusion, “but rather the conclusion of emotional judgment.”
“Capgras delusions,” as psychiatrists eventually called the belief that loved ones have been replaced by identical imposters, are not just archival oddities. Our modern understanding of the disorder tells us much about how the brain has separate modules for analyzing the cognitive aspects of recognition, and for feeling the emotional aspects of familiarity. It shows us that while cognition and emotion can be neurobiologically dissociated, behavior makes a lot more sense when they’re left alone to intertwine.
As a contemporary neuroscientist, I see the history of Capgras delusions as a perfect example of the transformation of our thinking about the brain and behavior. The syndrome was, at first, the intellectual property of scientists for whom the mind had little to do with the brain. For them, Capgras delusions, like all delusions and everything else that would fall into the portfolio of psychiatry, was a metaphysical issue of mind and psyche.
But over this century, it has come to be recognized that every thought, emotion, or behavior is the direct end product of the material brain. The ways in which Capgras delusions are the product of such materialism tells us much about the differences between the thoughts that give rise to recognition and the feelings that give rise to familiarity. As we’ll see, these functional fault lines in the social brain, when coupled with advances in the online world, have given rise to the contemporary Facebook generation. They have made Capgras syndrome a window on our culture and minds today, where nothing is quite recognizable but everything seems familiar.
Madame M.’s delusions would seem to make perfect sense as a response to the trauma she experienced in her life. Amid her ravings about poisonings and abductions, four of her five children had indeed died in infancy. Given that reality, there could be things a lot worse than a protective delusional belief that your children are alive somewhere. But psychiatrists of the time weren’t oriented to the possibility of delusions arising from trauma that has produced a biologically damaged brain.
Instead, theorizing about the source of Capgras delusions took a psychodynamic turn. Freud had already declared in 1911 that delusions were caused by intensely repressed urges; this general flavor of interpretation was readily retrofitted for the specifics of Capgras delusions. By the 1930s, mainstream psychiatric opinion settled on a standard psychodynamic interpretation of Capgras delusions. Freudian dogma revolves, of course, around sexual repression, and the conflicting feelings of love and hate that we all carry concerning the people closest to us. In that framework, those who are not psychologically robust enough to handle such ambivalence succumb to Capgras—loved ones have to be split into a bad version (the imposter on the scene) and a good one (who has been abducted). Voila! (Except for having to explain why Madame M. happened to have unmanageably ambivalent feelings about most of the population of Paris, as well as about the doubles destined to have their own doubles.)
With the Freudian explanation in place, discussions about Capgras delusions often devolved into an issue of classificatory taste. Some viewed Capgras as a delusion all its own (with its own special psychodynamic causes). Others viewed it as simply one of an array of psychodynamically rooted “delusional misidentification syndromes.” Those included Fregoli delusions, where the sufferer believes that various people are actually the same person in disguise; Cotard’s syndrome, the belief that your blood or organs have been absconded with, or that you don’t exist at all; or reduplicative paramnesia, the sense that a familiar place has been copied and substituted. Meanwhile, other psychiatric savants who leaned toward taxonomic lumping merely clumped all these together with the garden-variety delusions that are secondary to psychosis.
For over half a century, Capgras delusions sat comfortably in the realm of psychiatry. In the 1960s and ’70s, it became clear the delusions can also occur in individuals with disorders such as schizophrenia and Alzheimer’s. This didn’t ruffle many classificatory feathers. After all, if your memory is declining to the point where loved ones are starting to be unrecognizable, your loved ones’ claims to kinship must seem pretty suspect, the acts of imposters. (My father, in the final stretch of a substantial dementia, once agitatedly shouted to my mother, “Where is my wife, my real wife, you’re not my wife, you’re some, er, some Communist!”) Dementia-related Capgras delusions were viewed as merely garden-variety delusions and confabulations that are secondary to cognitive failure, while any other examples remained endowed with psychodynamic meaning.
Capgras delusions, though, were about to come under the spell of one of the biggest revolutions in 20th-century medicine. It was spurred by the shock waves sent by the discovery in the 1950s that using a drug to block a certain type of neurotransmitter receptor was a lot more helpful to a schizophrenic than years of psychotherapy. This fostered the recognition that all behavior is rooted in biology, that aberrancies of behavior and neuropsychiatric disorders are as “real” biologically as, say, diabetes.
She summoned the police to aid her in rescuing a group of children locked in her basement.
Ironically, Capgras himself, in his earliest writings, briefly speculated that the delusions could reflect some sort of brain disease, before jumping on the psychodynamic bandwagon. Then an obscure paper in 1930 tentatively suggested the same, and was roundly ignored. It wasn’t until a spate of studies in the 1970s that two facts came to be appreciated.
First, if you examine the brains of people with Capgras delusions, you’ll often find clear evidence of brain disease. The appreciation of this came slowly, simply because the techniques available at the time—electroencephalography (EEGs), early generation brain scanners—picked up abnormalities in only a subset of individuals. But as more sensitive techniques came on board, such as functional brain imaging, it became clear that a substantial percentage of Capgras sufferers had organic brain diseases, usually centered around damage or atrophy of the frontal cortex.
This second fact was the flipside of the first: If the brain, particularly parts of the frontal cortical regions, were damaged, people would occasionally develop Capgras delusions.
A good example is seen in a 2013 study of a woman who had suffered an intracerebral hemorrhage in her right frontal cortex. After years of rehabilitation, she had mostly recovered function, having some residual spatial orientation problems. And while she readily recognized most people in her life, including her daughter and grandchild, she insisted that her husband had been replaced by an imposter. Yes, yes, she’d admit, he looks just like my husband, and he has been very helpful during my recovery, but he is most certainly not my husband; my husband is elsewhere. She readily identified pictures of her husband, but this man before her was not him. She also believed that her home had been replaced with an exact duplicate.
Capgras delusions had become the province of acute neurological insults. Discrete damage to the brain can produce someone who can identify the features of a loved one, yet who insists that the living, breathing person in front of them is an imposter. Which turns out to tell us a lot about one of the great false dichotomies about the brain.
Starting at least with Descartes, there has been the dualist distinction between “mind” and “brain,” or in a spinoff that has particularly engaged neuroscientists recently, between “cognition” and “emotion.” In the standard view, the latter two are functionally and neurobiologically separable, and are in some sort of perpetual, epic struggle over the control of your behavior. Moreover, this dichotomizing has typically given rise to the view that one of the two, in some sense a mixture of ethics and aesthetics, should dominate the other.
A dichotomy between cognition and emotion, we now know, is false, clearly explored in neuroscientist Antonio Damasio’s 1994 book, Descartes’ Error. The two endlessly interact, both functionally and neurobiologically. And most importantly, they’d better, because what we view as normal function requires extensive integration of the two.
This is seen when it comes to making decisions, especially in an emotionally aroused circumstance. Consider two key regions of the prefrontal cortex. First, there is the dorsolateral prefrontal cortex (dlPFC), one of the most egg-heady and “cognitive” parts of the brain; commensurate with that, it is the most recently evolved, and the slowest maturing brain region. Selective damage to the dlPFC produces someone who makes terrible decisions. Often this patient is impulsive, incapable of postponing gratification, and has an inability to shift his or her behavior in response to feedback. This is someone who, in a choice scenario, can verbalize the optimal strategy—“I know how this works, I’m going to wait for the second reward because it’s a lot bigger”—and then can’t stop themselves from choosing the lousy, instant payoff.
Meanwhile, there’s the “emotional” ventromedial prefrontal cortex (vmPFC), which is the conduit between the frontal cortex and the limbic system. Selective damage to the vmPFC produces someone who also makes terrible decisions, but of a different type. This person has tremendous difficulty deciding anything; he or she lacks any “gut” intuition in such matters. Moreover, the decisions tend toward cold, heartless pragmatism. When meeting someone, he might say, “Hello, I see that you are quite overweight,” and when chastised about it later, will respond with a puzzled, “But it’s true.”
When it comes to decision-making, particularly in a social context, what we view as appropriate behavior reflects a balance between emotion and cognition. What Capgras delusions show is that a similar balance occurs when it comes to identifying those whom we know best.
How do we identify a loved one? Well, he has eyes of a known color; distinctive hair texture; a particular posture; that scar on his chin from when he was a kid. Things we know. This is the purview of a highly specialized part of the primate brain, the fusiform gyrus, which recognizes faces, particularly those of significance.
But this is only half the story. How else do we identify the Significant Other? Well, we reimagine what it was like to hold her in our arms the first time; her scent from up close summons a thousand memories; we note her brief sardonic smile, knowing that it means she’s also bored by the dinner host. Things we feel. And this is the neurological purview of the “extended face processing system,” a diffuse network including a variety of cortical and limbic regions.
Identification is at the intersection of factual recognition and a sense of familiarity. In this framework, Capgras delusions arise when there is selective damage to the extended face processing network, impairing the sense of familiarity. Factual recognition is intact; you know that this person looks just like your loved one. But they just don’t feel familiar.
In the 2013 study, the woman with Capgras delusions about her husband, following her hemorrhage, underwent brain imaging while looking at pictures of familiar and unfamiliar people. In control subjects, both types of faces activated the fusiform face area, while familiar faces additionally activated brain regions associated with intention and the intersection of emotion and memory. And the woman with the delusions? She had normal activation of the fusiform, but no activation in the other regions. Her facial recognition was fine, while the emotional meaning of the face had evaporated.
But this only gets you halfway to the delusion. Suppose there’s one of those quirky moments where your Significant Other says or does something out of character, feels unfamiliar. Wow, that’s not like him, we think. We don’t then conclude, however, that he must have been replaced by an identical imposter. Instead, we find a more plausible explanation—it’s, say, because he didn’t get much sleep. The neurological damage that gives rise to Capgras delusions not only impairs the sense of familiarity, but also the reflective, evaluative capacities that would lead you to reject your imposter hypothesis as preposterous. Instead, Capgras sufferers often become hyper-detailed in their observations, as a means to confabulate an explanation for a world that makes little sense. Ah-ha, my Significant Other has a gap between his front teeth, but not as large as with this imposter. Nice try, buddy.
Capgras’ intact recognition but damaged sense of familiarity has a neurological flipside, something first emphasized in 1990 by Hadyn Ellis and Andrew Young in the United Kingdom. This is prosopagnosia, a defect seen with damage to the fusiform gyrus. People no longer recognize faces, including those of loved ones, celebrities or famous historical figures. This can be hugely troubling, and sufferers can grope their way back to the rudiments of normal function with the most mechanical algorithms of recognition. Ah, if this person visiting me in the hospital room has this shaped face, this particular birthmark, then it’s my spouse.
But the thing that makes acquired prosopagnosia the mirror of Capgras delusions is the fact that with the former, amid destruction of cognitive recognition, the affective sense of familiarity is still there. Show someone with prosopagnosia a series of faces—Nope, I don’t recognize this person, not that one either—with a picture of a loved in the sequence, and you will see the same disavowal—Nah, don’t recognize this one—but the autonomic nervous system responds to familiarity. Heart rate changes, galvanic skin conductance shifts. Recognition is shot, you insist you’ve never seen this face before in your life, but the affective circuitry of the brain knows exactly who it is—this is the one who makes me feel safe, whose smile and form and scent have greeted me each morning since we joined our lives.
. Chesnot/Getty Images
The terrible and complementary dislocations of Capgras delusions and prosopagnosia show what happens when you pry apart the conjoined balance of cognition and emotion. The separate modules of our brains underlie dissociable functions, but we rarely fare well when those functions are dissociated. The dissociation of cognition and emotion, of recognition and familiarity, is what makes Capgras delusions a metaphor for the state of our minds today.
How do we identify a loved one? This is the purview of the primate brain.
For 99 percent of hominid history, social communication consisted of face-to-face interactions with someone you’ve hunted and foraged with most of your life. But then the recognition and familiarity components got pried apart by modern technology. By “modern technology,” I mean a newfangled invention that came along a few millennia ago—you could communicate with someone by putting scratches of ink on a piece of paper, and then sending that paper a great distance where they’d decode it. Wait, you know someone by their microexpressions, their pheromones, their totality—not by implicitly assessing word frequency in their letter or the scrawl of their signature. This was a first technological blow to the usual primate sense of familiarity. And the challenges have accelerated exponentially from there. Is this text message from my loved one, does it feel familiar? Well, it depends. What emoticon did they use?
Thus, not only has modern life increasingly dissociated recognition and familiarity, but it has impoverished the latter in the process. This is worsened by our frantic skill at multitasking, especially social multitasking. A recent Pew study reported that 89 percent of cell phone owners used their phones during their most recent social gathering. We reduce our social connections to mere threads so that we can maintain as many of them as possible. This leaves us with signposts of familiarity that are frail remnants of the real thing.
This can lead to a problem; namely that we become increasingly vulnerable to imposters. Our social media lives are rife with simulations, and simulations of simulations of reality. We are contacted online by people who claim they know us, who wish to save us from cybersecurity breaches, who invite us to open their links. And who are probably not quite who they say they are.
By any logic, this should induce all of us to have Capgras delusions, to find it plausible that everyone we encounter is an imposter. After all, how can one’s faith in the veracity of people not be shaken when you sent all that money to the guy who claimed he was from the IRS?
But something very different has occurred instead. This withering of primate familiarity in the face of technology prompts us to mistake an acquaintance for a friend, just because the two of you have a Snapchat streak for the last umpteen days, or because you both like all the same Facebook pages. It allows us to become intimate with people whose familiarity then proves false. After all, we can now fall in love with people online whose hair we have never smelled.
Through history, Capgras syndrome has been a cultural mirror of a dissociative mind, where thoughts of recognition and feelings of intimacy have been sundered. It is still that mirror. Today we think that what is false and artificial in the world around us is substantive and meaningful. It’s not that loved ones and friends are mistaken for simulations, but that simulations are mistaken for them.
Robert Sapolsky is a professor of biology, neurology, and neurosurgery at Stanford University, and author of A Primate’s Memoir and Why Zebras Don’t Get Ulcers. His newest book, Behave: The Biology of Humans at Our Best and Worst will be published in the spring.