Part of the problem in the psychosurgery movement was that Moniz, Freeman, and other surgeons reported their own results, with little or no external verification. They were, of course, inclined to view their surgeries as successes and to downplay the negative outcomes. The proper evaluation of any brain operation requires, at a minimum, that the patients’ cognitive abilities be tested before and after surgery to determine whether their capacities are affected by the insult to the brain. Ideally, patients should be tested by an independent psychologist who has no vested interest in the outcome, and in a way that allows for the patients’ psychiatric and cognitive functioning to be quantified using standardized tests. The tests should be used to track how a patient’s disease progresses over time—for better or for worse.
During the heyday of psychosurgery, few patients were given this kind of scientific scrutiny. More often, the patients’ physicians, with some input from the patients’ families, judged the success or failure of an operation based on subjective observations. For many of the families, any signs that the patient’s behavior had improved may have been so welcome that other side effects, such as loss of memory or cognitive skills, were overlooked or accepted as a trade-off for improvement. Although these assessments were far from rigorous, the success stories were accepted—sometimes exalted—by the medical community, published in scientific journals, and heralded by the media.
Nevertheless, by the late 1950s it became clear that lobotomies were hazardous. The most tragic consequences included death, suicide, seizures, and dementia. Freeman himself recognized a lobotomy syndrome that could arise from the operation, with symptoms including loss of creativity, inability to react appropriately to environmental cues, bedwetting, sluggishness, and epileptic convulsions resulting from scar tissue that formed in the brain after the operation. The number of lobotomies gradually dwindled due to growing concern in the medical and scientific communities.12
In the later twentieth century, newly synthesized antipsychotic medications such as chlorpromazine, antidepressant medications such as imipramine, and psychotherapy began to replace psychosurgery as a form of treatment. In the 1970s, the National Commission for the protection of Human Subjects of Biomedical and Behavioral Research gathered and examined data on the effects of psychosurgery, and concluded that psychosurgical procedures should not be completely prohibited but can be performed only under certain circumstances in which the patients’ rights and safety are protected. Psychosurgeons, once the stars of academic psychiatry, eventually became outsiders in the field.13
At the time of Henry’s operation, psychosurgery was still in vogue. Still, many neurosurgeons, aware that symptoms remained after frontal lobotomy, had begun hunting for psychosurgical variants, seeking areas outside the frontal lobes that supported mechanisms underlying mental breakdown and recovery. Many researchers set their sights lower and deeper in the brain. Frontal lobotomy entailed cutting connections beneath the frontal lobes willy-nilly, whereas new procedures targeted limited brain areas.
Scoville was among the neurosurgeons developing these alternative procedures. Although he had performed frontal lobotomies in forty-three psychotic patients during the 1940s, Scoville suspected that the frontal lobes were not the seat of psychosis or the best target for curing it. He believed instead that the positive results reported for psychotics who underwent frontal lobotomies were due to the patients’ reduced anxiety rather than a true change in their psychoses. Scoville, therefore, turned his focus to the inner part of the temporal lobes, which seemed to hold greater hope for curing patients. He became interested in this part of the limbic system, a set of structures underneath each cortical hemisphere, because it was believed to be the seat of emotion in the brain.
Scoville set out, as he put it, on a “project of direct surgical attack” on this part of the brain, devising a new surgical technique he called medial temporal lobotomy. In 1949, he began performing lobotomies focused on the limbic system. He carried out several versions of his operation, typically in female patients who were confined to state hospitals in Connecticut. Most of them were severely disturbed schizophrenics, but two patients were described as mentally deficient with psychosis and epilepsy. Scoville’s procedure was intended to address the psychosis only; psychosis and epilepsy are distinct maladies, caused by different abnormalities of the brain, so it was just a coincidence that these two women suffered both. After Scoville operated on the women, their epileptic seizures became less frequent and severe; one woman showed a slight reduction in her psychiatric symptoms, and the other showed marked benefit. The seizure relief was a serendipitous finding that prompted Scoville to investigate whether temporal lobe surgery could be a treatment for epilepsy. In 1953, he published the results of the operation on the two women (and seventeen others) and operated on Henry the same year.14
Scoville was not alone in seeing a connection between the temporal lobes and epilepsy. Earlier studies had found that electrically stimulating temporal-lobe structures could provoke epilepsy-like symptoms in animals; the same was true when epileptic patients undergoing brain operations received electrical stimulation in these regions. In the early fifties, Wilder Penfield, an eminent neurosurgeon at the Montreal Neurological Institute, began performing operations removing tissue from the left or right temporal lobe of patients afflicted with seizures.15
In this context, Scoville recommended medial-temporal lobotomy for Henry. Because of the severity of Henry’s epilepsy and the inability to control it, even with high levels of medication, Scoville thought he would be a good candidate for what he later called a “frankly experimental operation.” He hoped that by removing a significant portion of the medial temporal lobes, he would finally be able to keep Henry’s seizures at bay.16
Viewing the brain from the side, we see how the bulge of the frontal lobes, which fills the space behind the forehead, curves down and meets a smaller bulge lower in the brain. Scoville aimed for the inner part of this lower bulge, the temporal lobes. Gaining access through one of the holes drilled in Henry’s skull, Scoville made a cut in the dura. He exposed the shiny and convoluted surface of the brain, crossed with bright red blood vessels. The brain pulsed lightly, in time with Henry’s breath and heartbeat. Scoville’s entry was near the optic chiasm—the area where nerve bundles running from each eye cross one another and travel to the opposite side of the brain. He inserted a long, thin brain spatula underneath one frontal lobe, lifted it up, and moved aside the large blood vessels that wrapped around the brain’s surface. An assistant handed him a suction device to remove any excess blood or cerebral spinal fluid, and an electrical device to cauterize any leaking blood vessels. As he raised the frontal lobe from the lower part of the brain and spinal fluid leaked out, the brain sank down in the skull, giving Scoville more room to work. He could now see the uncus, the front part of the hippocampus. The uncus, meaning “hook,” resembles a fist at the end of a bent wrist. Scoville had previously found that delivering even weak electrical stimulation to this structure in conscious patients caused seizures, providing a rationale for removing it to treat epilepsy (see Fig. 2a and Fig. 2b).17
To perform the resection, Scoville used a technique called aspiration, in which he guided a small instrument through the hole in Henry’s bone and into the medial temporal-lobe region. He then applied fine suction, and with that simple action, pieces of Henry’s brain were sucked into the device bit by bit. Scoville extracted the uncus, the front half of the hippocampus, and some neighboring cortex, including the entorhinal cortex. He also removed most of the amygdala, which hugs the hippocampus and is critical for expressing and feeling emotions. Having finished his work on one side of Henry’s brain, Scoville repeated the procedure on the other side.18
The holes in Henry’s skull allowed Scoville to see what he was doing, but it was still impossible to know exactly how much tissue he had extracted. Later MRI studies showed that he had overestimated the extent of the removal—he believed it was eight centimeters of tissue o
n each side, but the actual area missing from Henry’s brain was slightly more than half that.19
In the course of the operation, Scoville removed the inner part of the temporal pole; most of the amygdaloid complex; the hippocampal complex, except for about two centimeters at the back; and the parahippocampal gyrus—entorhinal, perirhinal, and parahippocampal cortices—except for the back two centimeters. The brain has a left hippocampus and a right hippocampus, located above each ear deep in the temporal lobes. Pathways that cross the middle of the brain from left to right and right to left interconnect the two hippocampi. Because of Henry’s case, we now know that damage to the hippocampus on both sides of the brain causes amnesia, but in 1953, scientists did not understand that the capacity for memory formation was localized to this particular area. This lack of evidence led to Henry’s tragedy, and studies of his condition filled this gap in knowledge.
Before the 1930s, anatomists believed that the main function of the hippocampus was to support the sense of smell, and no one knew that a memory network occupied this structure. But scientists had written about the role of medial temporal-lobe structures in emotion. James Papez’s 1937 paper “A Proposed Mechanism of Emotion” described what came to be called the Papez circuit: a ring of structures, including the hippocampus, that are anatomically connected and provide a mechanism for feeling and expressing emotion. In 1952, Paul MacLean introduced the concept of the limbic system, which included the amygdala, calling it the emotional brain. Scoville and his colleagues must have known about the central role of medial temporal-lobe structures in emotion when they carried out their medial temporal lobotomies.20
For Henry, the effect of removing the front half of the hippocampus was the same as if Scoville had sucked out the entire structure. The remaining two centimeters—roughly three-quarters of an inch—were deprived of input from the outside world and therefore nonfunctional. The major route by which information reaches the hippocampus is via pathways in the entorhinal cortex, which Scoville also removed. Thus, new information from vision, hearing, touch, and smell would not be able to reach the residual hippocampus.
Throughout the operation, an anesthesiologist carefully monitored Henry’s condition. In such procedures, brain surgeons worry about damaging critical functions, such as movement and language. By asking Henry to squeeze his hand, the anesthesiologist could test both Henry’s ability to understand language and his capacity to move. Although he remained conscious during the surgery, Henry was likely given sedatives to keep him from becoming restless.
When Scoville finished the removal, the anesthesiologist gave Henry a general anesthetic so he would not feel anything as Scoville completed the procedure. He stitched together the cut in the brain’s outer membrane, replaced the disks of bone in Henry’s skull, and sewed his scalp back together.
After the operation, Henry was taken to a recovery room, where doctors and nurses watched him closely to make sure that no life-threatening problems, such as hemorrhage, arose. Nurses checked his vital signs at fifteen-minute intervals until he was awake and clearly out of danger. They then took him back to his hospital room, where his parents were able to visit him.
In the days that followed, Henry was drowsy but otherwise seemed to make a good physical recovery from the ordeal. It soon became clear, however, that something was terribly wrong. Patients recovering from brain surgery often experience a period of confusion, but Henry’s condition went far beyond that. He did not recognize the caregivers who came to his room every day or recall the conversations he had had with them, and he could not remember the day-to-day routines of the hospital. When Henry could not find his way to the bathroom despite having been there several times before, Elizabeth Molaison began to realize that something tragic had happened.
Under questioning by his family and hospital staff, Henry could recall some small events just before the time of his operation, but he did not seem to recall anything of his time in the hospital. He could not remember the death of his uncle three years prior or other momentous events in his life. By the time he left the hospital, two and a half weeks after his operation, it was clear that Henry suffered from severe memory impairment—amnesia.21
The operation, however, did in fact accomplish what Scoville had hoped. Henry’s seizures were dramatically curtailed, but this benefit came at a devastating cost. Elizabeth and Gus, who always had to take care of Henry because of his seizures, now found themselves with a son who could not remember what day it was, what he had eaten for breakfast, or what they had said just minutes before. For the rest of his life, Henry would be trapped in a permanent present tense.
Three
Penfield and Milner
After his operation, Henry might have continued to live a difficult but private life under the devoted care of his parents. But his case soon attracted the attention of the scientific community, hungry for knowledge about the human brain. From his tragedy, we learned that our brains are capable of carrying out many different computations related to memory as it is formed, consolidated, and retrieved in numerous, specialized brain circuits.
Henry was not the first person to develop a severe, long-term memory impairment following a brain operation to relieve epilepsy. Around the same time, two other men, F.C. and P.B., suffered a similar plight. Both men were amnesic immediately after operations performed by Wilder Penfield, the founder and director of the Montreal Neurological Institute at McGill University. Penfield had removed part of the left temporal lobe in each patient to alleviate epileptic seizures.1
Penfield, along with then McGill graduate student Brenda Milner, studied both F.C. and P.B. extensively. Milner later studied Henry as well. Their research was part of a growing movement among scientists to link complex mental abilities, such as memory and cognition, to specific anatomical structures in the brain. These three remarkable cases—F.C., P.B., and H.M.—provided a quantum leap in neuroscience and formed the basis of modern memory research.
Henry’s story is inextricably linked to the extraordinary life of Penfield and his institute. Penfield was born in Spokane, Washington, in 1891. His father and grandfather were physicians, and he followed in their path. After attending a private high school for boys, he studied at Princeton University and later began medical school at the College of Physicians and Surgeons in New York. But Penfield’s plans changed after six weeks. His academic achievement, athletic prowess, and social success won him a Rhodes Scholarship, and in 1914, at age twenty-four, he entered Merton College at Oxford University in England.
My brief account of Penfield’s life draws heavily from his autobiography. He studied both science and medicine, and this dual training established his lifelong passion for bridging the two disciplines. From the outset of his studies, Penfield worked under giants in these fields. During his first two years at Oxford, his mentors were Sir Charles Scott Sherrington, winner of the Nobel Prize for Physiology or Medicine in 1932 for his discoveries on the function of neurons, and Sir William Osler, architect of bedside teaching and the medical residency system.2
After completing his fellowship at Oxford, Penfield returned to the United States and finished his last year of medical school at Johns Hopkins University. Following a surgical internship in Boston at the Peter Bent Brigham Hospital, under the famous neurosurgeon Harvey Williams Cushing, Penfield returned to England for two years of graduate study, pursuing neurophysiology in Oxford and neurology in London at the renowned National Hospital at Queen Square.
In 1921, Penfield returned home, and at age thirty, with unrivaled schooling, he accepted a position at the Presbyterian Hospital in New York for training in neurological surgery. There he made his initial venture into neurosurgery. His first patient was a man with a brain abscess, a mass filled with pus. The second was a woman with a brain tumor. Both patients arrived at the hospital in comas, and despite Penfield’s heroic attempts in the operating room to save them, both died. Although depressed by these failures, Penfield believed that the practice of brain surge
ry would make enormous leaps during his lifetime.
The focus of Penfield’s teaching and research was the examination of tissue he had removed from patients’ brains during surgery. He hoped that through his microscope, he would see something to provide clues about the cause of epilepsy. His results were disappointing, however, because his methods could not capture sufficient detail in the cells. Around that time, he had the good fortune to read an article in a Spanish journal that included drawings of brain cells, in which the different parts of each cell stood out sharply. The author of the article was Pío del Río-Hortega, a Spanish researcher at Madrid’s Cajal Institute, and Penfield was eager to visit his laboratory. In 1924, he received permission from his department to go to Spain for six months to visit Río-Hortega’s lab. There, Penfield worked on a fundamental problem that faced biologists: how to identify specific types of cells.
When researchers look at brain tissue through a microscope, they see a complex and mysterious array of structures. The brain has many different kinds of neurons, which are specialized for different functions. But as important as neurons are, glial cells far outnumber them. Glia—Greek for glue—provide structural support for neurons, and, in Penfield’s day, were believed to be unimportant for the transmission of nerve impulses. We now know, however, that they are active partners with neurons, and that the interactions between these two cell types are likely vital to the function of synapses, the gap across which one neuron sends messages to the next.
Researchers often study neurons and glia by injecting stains that are taken up by a specific kind of cell, making it stand out from its neighbors. In Madrid, Penfield helped pioneer this technology with Río-Hortega, who had developed advanced methods for staining brain tissue as a tool for uncovering the structure of nerve cells and their connections. Under Río-Hortega’s guidance, Penfield produced the first reliable stain for a kind of glia called oligodendroglia, and described them in a 1924 publication. Because these cells appear in response to brain disease or injury, being able to identify them gave neuropathologists a method for examining abnormal brain tissue.3
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