For most of human history, personality was thought to be a stable thing. A person had a character, and that character was theirs. It might be shaped by upbringing, by circumstance, by the moral choices they made across a lifetime, but it was, at some level, who they were. Injury, illness, and misfortune could damage the body. What sat underneath the body, the person themselves, was thought to be something more durable than that.
Then a foreman named Phineas Gage was working on a stretch of railway line in Vermont, and an accidental blast sent a three-and-a-half-foot iron rod straight up through his cheek and out the top of his skull. He survived. He returned to consciousness within minutes. He talked to the doctors, described what had happened, and went on to live for another eleven and a half years.
What he did not do was return to being the man his colleagues had known before the accident. And the specific way in which he did not return has, on the accumulated evidence of nearly two centuries of neurological research since, quietly transformed our understanding of what human personality actually is.
What the case demonstrated
According to Dr Malcolm Macmillan of the University of Melbourne, writing in the British Psychological Society’s journal The Psychologist in September 2008, Dr John Martyn Harlow, the physician who treated Gage, published a second report on the case twenty years after the accident. In fewer than two hundred words, Harlow described what had happened to the man Gage had once been. The balance between his intellectual faculties and his animal propensities had been destroyed. He had become fitful, irreverent, grossly profane. Impatient of restraint. Obstinate and capricious about his plans for the future. A child intellectually, Harlow wrote, with the animal passions of a strong man. His friends and family, so radical was the change, said he was no longer Gage.
The specific scientific implication of that observation, taken seriously, was disturbing enough that most of Harlow’s contemporaries could not accept it. What the case proved, on the strongest current reading, was that the specific patterns of behaviour, self-control, judgement, moral conduct and social feeling that we recognise as a person’s character are not distributed across some abstract quality of the self. They are located in a specific, small, physical region of the brain. Destroy that region, and the person who existed inside it does not survive. The body walks out of the surgery. The person does not.
For most of the nineteenth century, this proposition sat in the medical literature as an isolated curiosity, easily dismissed as an anomaly of one man’s injury. The reason it can no longer be dismissed is that the twentieth and twenty-first centuries have produced enough additional cases to establish it as a general rule of human neurology.
Watch this short video to learn more about this fascinating story:
The modern name for what happened to Gage
In 1985, the American neurologists Paul Eslinger and Antonio Damasio published the case of a patient they identified in their reports by his initials, EVR. EVR had been a comptroller at a home-building firm, married with children, professionally successful, socially unremarkable. A benign tumour was discovered near his frontal lobes, and it was surgically removed. The operation was successful in the sense that the tumour was removed cleanly and EVR retained normal intelligence, normal memory, and normal language function.
What EVR did not retain was the capacity to make sound decisions about his own life. Over the following years, according to the clinical follow-up documented by Eslinger and Damasio, he made a series of increasingly poor judgements at work, was eventually dismissed, made further increasingly poor judgements in his personal life, went bankrupt, and was abandoned by his wife and friends. His cognitive tests remained within normal limits throughout. What had been damaged, on the accumulated evidence, was the specific system in the human brain that assigns emotional weight to future consequences and translates that weight into present-day judgement.
Eslinger and Damasio coined a specific clinical term for what had happened to EVR. They called it acquired sociopathy. The medical literature now uses the term to describe a specific and well-characterised syndrome in which an adult with previously normal personality, judgement and social conduct develops the specific pattern of impaired empathy, impaired guilt, impaired long-term planning and impaired social judgement that clinical psychiatry ordinarily associates with a psychopathic personality, following focal damage to the ventromedial prefrontal cortex.
According to a 1999 paper by Steven Anderson, Antoine Bechara, Hanna Damasio, Daniel Tranel and Antonio Damasio in the journal Nature Neuroscience, the same specific pattern has been documented across dozens of cases in the medical literature. What the cases collectively demonstrate is that the human capacity to feel guilt, to plan for future consequences, to hold long-term commitments to other people, and to experience the pattern of moral feeling that most of us regard as central to being a person, is dependent on the physical integrity of a small region of tissue behind the eyes. That tissue can be damaged in an accident, removed during surgery, deprived of oxygen during a stroke, or slowly destroyed by a degenerative disease. In all four cases, the person the patient had been before the damage does not, on the accumulated clinical evidence, come back.
What this looks like in the ordinary world
What made Gage’s case exceptional was the specific dramatic mechanism, an iron rod through the head, which meant the injury and the resulting personality change happened in a single afternoon that could be photographed and remembered. The reason the same syndrome is not, in ordinary experience, considered a common medical event is that its most frequent modern cause is not accidental at all. It is a specific form of dementia, and it unfolds slowly enough that most families do not recognise what is happening until years after it has begun.
According to the clinical materials published by the University of California San Francisco Memory and Aging Center, behavioural variant frontotemporal dementia, or bvFTD, is a progressive neurodegenerative disorder that primarily affects the frontal and temporal lobes of the brain. It typically presents in adults between the ages of 50 and 60. Its earliest and most characteristic symptoms are, in almost every respect, the same syndrome that Harlow observed in Gage and Eslinger and Damasio observed in EVR.
The patient loses empathy for the people closest to them. They lose interest in personal hygiene and appearance. They stop caring about family relationships, friendships, and long-standing commitments. They may act inappropriately toward strangers, break rules they had followed all their lives, spend money recklessly, and, in a subset of cases, commit criminal offences of a kind that would have been unthinkable to them before the disease began. The specific psychological quality that families most consistently describe as the first sign, on the clinical caregiver literature, is not memory loss. It is the sensation, unfolding slowly over months or years, that the person they married or the parent who raised them has been replaced by someone who looks identical to them but does not feel like the same person.
Families describe this in almost identical language across independent case reports. The affected spouse becomes emotionally cold, distant, or reckless. The parent stops recognising the moral significance of what they are doing. The affable colleague becomes indifferent to consequences. What the disease is doing, on the strongest current reading of the neuroanatomy, is quietly performing the same procedure that a three-and-a-half-foot iron rod performed on Gage in 1848, only slowly, and without any dramatic event to point to.
What the accumulated evidence implies
The uncomfortable proposition that follows from all of the above, taken seriously, is not that some people have fragile personalities and others do not. It is that human personality itself, as a general phenomenon, is contingent on the intact functioning of specific brain tissue that any human being can lose, at any time, through any of several mechanisms none of us fully control.
The kindest person we know is kind because a specific network of neurons in the ventromedial prefrontal cortex is working correctly. The most reliable colleague is reliable because a specific circuit in the orbitofrontal cortex is generating the specific emotional signals that make future consequences feel real in the present moment. The parent who has spent thirty years attending to the wellbeing of their children is doing so because the specific machinery that assigns emotional weight to other people’s welfare is, at this moment, physically intact inside their skull.
None of that machinery is permanent. Any of it can be damaged by trauma, disease, surgery, stroke, tumour, or the slow protein accumulations that produce frontotemporal dementia. On the accumulated clinical evidence of the past four decades of neuroscience, the specific person who existed before the damage does not, in most documented cases, return.
What the case of Phineas Gage first named, on the strongest current reading of the medical record, is a proposition that most of us prefer not to think about at length. The people we love are not, in any biological sense that modern neuroscience can support, permanent. Their kindness, their steadiness, their moral character, and the specific set of feelings and judgements that make them the specific person we know, are being maintained, moment by moment, by a small volume of physical tissue that could fail. In most lives it does not fail catastrophically. In some lives it does. What Gage’s story, and every clinical replication of it since, has quietly established is that the difference between the two cases is not moral. It is anatomical.
That is what the accident in Vermont in 1848 actually proved. It has taken most of the intervening 178 years for the implication to be accepted, and, on the current state of the neurological literature, most families still encounter it for the first time when it happens to someone they love.
