The letters were between my grandfather and two Harvard scientists—the endocrinologist Fuller Albright and the neurologist Stanley Cobb—and they gave a glimpse of my grandfather’s early ambitions, as well as some of his motivating impulses. He had written most of the letters while he was a neurology intern at Bellevue Hospital in New York City, exploring his next steps. He wanted, he wrote in his first letter to Albright, “advice and possible help in getting some first-hand experience in clinical endocrinology, especially as related to a neurological-psychiatric practice.” Endocrinology is the study of the endocrine system, which regulates the body’s hormones. He enclosed a copy of his only publication at the time, a solipsistic case study from the Journal of the American Medical Association chronicling his own bout with an at-first-mysterious illness. “A physician,” the paper reads, “aged 28, in the summer of 1934, after drinking raw cow’s milk and eating goat cheese in Norway, developed periodic exacerbations of malaise, easy fatigability, and generalized muscle and joint pains.” He describes how the aching and exhaustion had laid him low for six months, causing him to put his young career on hold and leading to multiple diagnoses of neurasthenia, a catchall psychiatric term that at the time was often applied to describe people who were simply unable, mentally, to cope with high levels of stress. The paper chronicled his attempts to find an alternate explanation and ended with his discovery that he tested positive for brucella, an undulant-fever-causing bacteria carried by cows and goats in, among other places, Norway. The paper’s single illustration was a black-and-white photograph of my grandfather’s pallid forearm displaying a large abscess that a diagnostic skin test had provoked. He clearly relished proving his physicians wrong and finding a simple, easily treated, biological cause for what they had attributed to a vague and hard-to-target mental condition. “This paper,” he wrote in the closing comment, “suggests one more substitute for that diagnostic wastebasket ‘neurasthenia.’ ”
In the letter to Albright, my grandfather outlined the career path he’d followed so far: “I attended Yale College, B.A. 1928, Univ. of Penn medical school 1932, two years of general medicine and surgery at the Hartford Hospital and the Presbyterian medical center NYC; one year in psychiatry at the Cornell Medical center; and one year in neurology under Dr. Foster Kennedy at Bellevue Hospital.” Kennedy, incidentally, was an aggressive proponent of eugenics, who in 1942, while he was president of the American Neurological Association, raised eyebrows by arguing that people who suffered from mental retardation should be killed, declaring that “the place for euthanasia, I believe, is for the completely hopeless defective; nature’s mistake; something we hustle out of sight, which should not have been seen at all.”
Cobb and Albright offered my grandfather a yearlong dual fellowship, splitting time between Cobb’s clinical practice and Albright’s laboratory. My grandfather accepted with enthusiasm and agreed to move to Boston as soon as his contract with Bellevue expired. He was excited at the prospect of tackling important research, though he was worried that his enthusiasm might outstrip the constraints of time. “The problems of urine-assay of sex hormones in homosexuals or menopausal or pregnancy psychoses seems too vast and a bit impractical to list in an application for a year’s fellowship, don’t you think?” he wrote. In the meantime, he wrote, he was open to suggestions for any experimental endocrinological work he might conduct before he left Bellevue. He wondered whether there might be “a simple problem I might work at” while at the hospital, with its “wealth of material but poor laboratory facilities.”
I had to read it twice before I understood what he meant by “material.”
The dual fellowship with Cobb and Albright did not end up being particularly successful. After reviewing some of the research reports my grandfather produced in Albright’s lab, Albright wrote to him that “I have been over your manuscripts. The problem with them is this: they contain a lot of different problems but not quite enough observations on any one problem to absolutely clinch it. I feel that there is very little in them which would materially help the progress of medical science.” My grandfather didn’t object to the harsh critique: “Thank you for your kind and clear letter re my various articles and data. I quite agree that they constitute a hodge-podge of information of no great value,” he wrote.
But his stint with Cobb and Albright was fruitful in another way, since it was during this time that he discovered his passion for neurosurgery. Albright’s laboratory was located at Massachusetts General Hospital, which had a peerless neurosurgery department, and in his free time my grandfather took the opportunity to observe some of the best neurosurgeons in the world at work. He was captivated by what he saw and decided to apply for a neurosurgical residency there, which began the following year, in 1938. He proved a quick study. After a whirlwind of additional residencies at the Boston City Hospital and Johns Hopkins, he founded his own department of neurosurgery at Hartford Hospital in 1939.
He kept in touch with Cobb and Albright, even as their careers diverged. He’d write to them on his Hartford Hospital stationery, telling them about the milestones in his life. “Emmie just had a 7 ½ pound boy, with a magnificent Jewish nose,” he wrote to Albright upon the birth of my uncle Peter, his third child, in late 1939. Albright wrote back, offering his “congratulations on the new prophet which has arrived in your house.” He also let his former bosses know about any new material he came across that might be of interest to them. That same year, for example, he informed Albright about a twenty-eight-year-old man who presented a “beautiful picture of true pituitary hypofunction….It is impossible to guess his age. He has a soft skin, a high voice, no facial nor body hair, long legs, asthenic habitus, low blood pressure, no libido, etc., etc.” The following year, he wrote to inform him of a similar case, “a twenty-one-year-old dwarf who looks and acts as if he were in his early teens….His genitalia is about one-half adult size, his pubic hair is abundant but silky and in feminine distribution….Development and skeleton is symmetrical except for all structures being smaller than normal. Height approximately 3 feet 10 inches or so.”
At the end of that letter he asked his old boss a question. “Are you interested in having him on your experimental ward for study?” He noted that the dwarf was “cooperative and passive” and told Albright to write back “if you want us to send him up.”
—
The broken illuminate the unbroken.
An underdeveloped dwarf with misfiring adrenal glands might shine a light on the functional purpose of these glands. An impulsive man with rod-obliterated frontal lobes might provide clues to what intact frontal lobes do.
The history of modern brain science has been particularly reliant on broken brains, and almost every significant step forward in our understanding of cerebral localization—that is, in discovering what functions rely on which parts of the brain—has relied on breakthroughs provided by the study of individuals who lacked some portion of their gray matter.
This had not always been the case. Until the nineteenth century, most scientists viewed the brain as an undifferentiated mass. They recognized its importance, understood that it was the seat of emotion and intellect and consciousness, that it mediated our senses, that it more or less was us, but the reigning theory of brain function held that the brain was a perfect democracy, where every part was equal in potential and capability to every other part. From this view, injury to a particular part of the brain would simply cause a generalized diminishment of function, rather than any specific deficit. The movement away from this view faced a lot of resistance. One reason for this was the rise of phrenology, a pseudo science that became a worldwide fad in the mid-1800s and held that people’s personalities and intellects could be minutely described simply by running your fingers over their heads and reading the contours of their skulls, which reflected the dimensions of the brains they encased. Phrenologists believed in cerebral localization, but the problem was, their arguments and theories about that localization had more in common wit
h astrology than astronomy. The eventual debunking and stigmatization of phrenology made real scientists wary of accepting the reality of cerebral localization until inescapable evidence for it began to emerge in the form of brain-damaged individuals.
Phineas Gage was pivotal.
Then, in 1861, the year after Gage’s death, a French neurosurgeon named Pierre Broca wrote a paper describing a new patient who was, in many ways, more scientifically significant than Gage. The patient’s name was withheld, but he came to be known in the literature as Monsieur Tan, owing to the fact that he could not speak with any coherence and was able to say only the word tan over and over again. He had maintained his other faculties, however, and was able to understand everything he heard, and write legibly and intelligently. Upon the patient’s death, Broca performed an autopsy and discovered that Monsieur Tan had a small and sharply circumscribed lesion in a small part of the left hemisphere of his inferior frontal lobe. He surmised, correctly it turns out, that this region of the brain was crucial for speaking. Today all basic human anatomy courses identify that spot corresponding to the damage in Monsieur Tan’s brain as Broca’s area, the center for speech articulation. (Monsieur Tan’s brain, incidentally, went on to find a home in another museum of anatomical curiosities, this one located in Paris.)
Seventeen years later, in 1878, Carl Wernicke, a German neurologist, described a patient with damage to his posterior left temporal lobe, a man who spoke fluently but nonsensically, unable to form a logical sentence or understand the sentences of others. If Broca’s area was responsible for speech articulation, then Wernicke’s area, as it came to be known, must be responsible for language comprehension.
And so it went.
The broken illuminated the unbroken.
Among brain scientists, this approach, teasing out the functions of different areas of the brain by studying individuals who lacked those areas, became known as the lesion method, and by the middle of the twentieth century, it had become predominant. The notion that different areas of the brain corresponded to different functions was no longer controversial; it had become universally accepted dogma. Bit by bit, area by area, scientists were plotting out a functional map of the human brain.
But that map still contained immense expanses of uncharted territory.
For example, scientists might have succeeded in pinpointing a dime-size portion of the brain’s superior temporal plane as necessary for the in-the-moment perception of sounds, and labeled it the primary auditory cortex, but they had no clue what part of the brain was responsible for our ability to recall and recognize a specific sound at a later date. Or, for that matter, how it could do the same for past sights or tastes or touches or smells or the multisensory stews that constitute human experience.
The brain was slowly giving up some of its secrets, its ancient functions coming to light, but memory, which more than anything else defines us, remained a dark mystery.
—
In the basement of the library, right before I took the elevator up to the fifth floor and stumbled on Phineas Gage, I read one of the earliest letters from my grandfather to Fuller Albright. In it he described some of his long-range goals.
“I have done no animal or experimental work since being a medical student in physiology and helping a little in the experimental surgery department,” he wrote, “but my chief hobby is mechanics, so the technical side of research appeals to me strongly.”
He wrote the letter in 1936. Within a decade, he would find a way to unite his passion for tinkering and his interest in experimental surgery.
And, in the back wards of asylums around the country, he would discover a nearly limitless source of material.
TEN
ROOM 2200
He drove the twenty miles from Hartford to Middletown in his new Buick convertible, top up to shield him from the approaching New England winter, following the highway alongside the Connecticut River due south and pulling off just before the river veered southeast toward the ocean. Middletown was once the largest and most prosperous city in Connecticut, a bustling port where traders made fortunes provisioning the Caribbean colonies with goods and slaves. Once the business of slavery declined, the residents found new purpose, building factories to assemble Colt firearms and Royal typewriters, and founding Wesleyan University, a liberal arts college on the west side of the city. Wesleyan was the city’s most well-known institution, but on the opposite side of town was a second institution, built around the same time and almost double its size. That’s where my grandfather was heading. It was November 14, 1946. He could see the redbrick and wrought-iron gate of the asylum on a hill in the distance long before he got there.
As he passed through the gate, my grandfather might have noted some similarities between Connecticut State Hospital and his wife’s asylum, the Institute of Living. Both made good first impressions, and although the grounds at the asylum in Middletown weren’t designed by Frederick Law Olmsted, they too were beautiful. The largest building, Shew Hall, towered at the head of a sloping circular drive and looked reminiscent, in architecture and scale, of Paris’s Élysée Palace, the residence of the French president. This was the asylum’s administration building, and from his office on the top floor the superintendent, Dr. Edgar C. Yerbury, could gaze west over all of Middletown, while the vast grounds of his institution sloped gently down toward the river to the east.
The Connecticut State Hospital was the largest public asylum in the world. It occupied 906 acres, 406 of which were taken up by the asylum’s farm, with its piggery, chicken coops, and verdant rolling pastures full of cows. Although the patients worked the farm for free, and the profits could be considerable—the previous year more than fifty thousand dollars of asylum-sourced milk was sold to the local community—the asylum as a whole was struggling. The problem was this: There were too many inmates. Every year the asylum was tasked with feeding and sheltering and protecting—from each other and from themselves—growing numbers of mentally ill men and women, but its resources had not kept pace. This pattern had been repeated all over the country in the 1940s as state asylums filled to overflowing. The cause of this insanity epidemic was a mystery. Some argued that it had to do with all the disturbed soldiers coming home from World War II. Others believed that the lingering anxieties and uncertainties provoked by the Great Depression had finally come home to roost, or that Americans were simply less willing and able to care for their disturbed relatives at home, as was once the norm, and had become accustomed to the idea of turning them over to the state.
Regardless of the reasons, state asylums nationwide were in crisis. And while conditions had been deteriorating for years, the general public had become aware of this deterioration only recently. In May 1946, Life published an exposé, “Bedlam 1946,” that hit newsstands with the force of an explosion. The text of the article painted a vivid picture of inmates being fed a “starvation diet” in “hundred-year-old firetraps in wards so crowded that the floors cannot be seen between the rickety cots.” But the text was nothing compared to the photographs. A man named Jerry Cooke had spent weeks in a state asylum in Ohio and emerged with a horrific portfolio of images straight out of a Hieronymus Bosch painting. On one page, a group of naked men huddled together against a wall, some hiding their faces in shame while others gazed hollow-eyed into the lens. On another page, an old woman, also naked, sat neglected and withered on a dilapidated wooden bench. To the American public, just emerging from World War II, the photos were both shocking and shockingly familiar. State mental hospitals, the country’s most popular magazine declared, had become “little more than concentration camps on the Belsen pattern.”
The article provoked not just outrage but action. Congressional hearings were held in Washington, and within two months of the magazine hitting newsstands, President Truman signed the National Mental Health Act, which provided federal funds for psychiatric research. There was broad consensus that the current conditions were untenable and that something had to be done t
o ameliorate them, although opinions varied widely about the best strategies for doing so. Was it a question of throwing more money at the asylums, increasing their carrying capacities? Or should more outpatient facilities be built, allowing potential patients to remain in their homes?
Or perhaps there was a simpler, quicker solution.
Perhaps there was a solution that took aim, with surgical precision, at insanity itself.
—
My grandfather parked his Buick in the visitors lot in front of Shew Hall, and no doubt Superintendent Yerbury came down to greet him. The day’s visit was a momentous one and had been almost a half year in the making. In June, just weeks after “Bedlam 1946” was published, Connecticut’s Joint Committee of State Mental Hospitals held a meeting in Hartford. The committee was an agency composed of the governing bodies of the state’s three public asylums: Connecticut State Hospital, Norwich State Hospital, and Fairfield State Hospital. While the Life exposé had not dealt specifically with these particular asylums, the article’s clear implication was that the horrors it depicted applied to state asylums nationwide, and the joint committee knew that it was in no position to rebut that view. The Connecticut state asylums, the committee would admit, were “seriously overcrowded, which, with the bad housing facilities, made it extremely difficult to render the best of service to our mentally ill patients.” Any measures that might reduce the numbers of inmates had to be examined, and it was clear that the time for action had arrived. At the meeting, Yerbury suggested that one solution might be for the three state asylums to adopt a “coordinated program of neurosurgery.” His peers agreed, and two months later, in August, representatives of all three state asylums met again to begin working out the details. That second meeting took place at the Institute of Living.
Although the Institute of Living, as a private asylum catering to the wealthy, didn’t face the same problems of overcrowding as its public counterparts, the latter had always looked to the former for guidance on the implementation of novel psychiatric treatments. The Institute of Living’s forward-looking superintendent, Charles Burlingame, presided over the meeting. He had already introduced the lobotomy on a limited scale at his asylum several years before, and my grandfather, as the Institute of Living’s chief consulting neurosurgeon, had performed the majority of them. In fact, my grandfather and several other neurosurgeons also attended that August meeting of the Joint Committee of State Mental Hospitals and “signified their willingness to be added to the state hospitals as consultants.” A third meeting was held a month later, on September 18, 1946, and this time several researchers from Yale attended. A general way forward was agreed upon: My grandfather and the other neurosurgeons would begin operating on patients at all Connecticut asylums, public and private, at least twice a week. Asylum personnel, overseen by researchers from Yale, would meanwhile keep tabs on the patients’ postoperative progress.
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