Stars in His Eyes

When Vincent van Gogh began painting a starlit sky one night, he found that “putting little white dots on a blue-black surface” failed to capture the vision before him. “It often seems to me that night is still more richly colored than the day, having hues of the most intense violets, blues, and greens,” he later wrote. “If only you pay attention to it you will see that certain stars are citron yellow, others have a pink glow, or a green blue and forget-me-not brilliance.”

It was the artist’s sensitivity to the nuances of hue that first drew Shahram Khoshbin, an associate professor of neurology at Brigham and Women’s Hospital, to van Gogh’s work. As a fine-arts student in Beirut, Khoshbin wrote his senior thesis on the painter’s florid use of tertiary colors, which emerge when a secondary color blends with a primary color.

“Through years of experimentation, van Gogh had discovered he could pair certain colors—such as blue-violet with yellow-orange—to evoke emotions,” says Khoshbin. “Such color combinations can trigger autonomic responses in viewers. When you stand before many of his paintings, your palms turn sweaty, your breaths come rapidly, and your heartbeat quickens.”

Despite his passion for art, Khoshbin ended up pursuing medicine instead. Yet that dichotomy didn’t last long. Soon his growing fascination with neurology led him to ponder van Gogh’s behavior as well as his art. Dozens of diagnoses—from schizophrenia to bipolar disorder, lead poisoning, and absinthe toxicity—had already been advanced to explain van Gogh’s vibrant paintings, eccentric life, and dramatic death. While a medical student at Johns Hopkins, though, Khoshbin seized the chance to ask a visiting lecturer about van Gogh’s diagnosis. “That’s simple,” replied Norman Geschwind ’51, a pioneer in behavioral neurology. “He had epilepsy, just like Dostoevsky.”

Khoshbin felt surprised, even after he learned that van Gogh’s own doctor had diagnosed the artist with epilepsy, because he doubted the disease could account for the full range of van Gogh’s symptoms. But an encounter the following year made that diagnosis resonate after all. While volunteering in the art-therapy program of a mental health facility, Khoshbin noticed that few of the patients used tertiary colors in their gouache paintings.

One evening, as he was helping the janitor tidy the studio, he mentioned his observation. The elderly man walked him downstairs to a closet filled with mops, buckets, and the rustling sounds of nesting rats. There the janitor extracted boxes of artwork he had collected over the decades. On the back of each of the hundreds of paintings he had inscribed the artist’s diagnosis.

“The schizophrenics’ artwork was meticulous and detailed,” Khoshbin remembers. “The depressed patients had splashed black and brown everywhere. But what stunned me was the box filled with art by the epileptics: In almost every painting they had used tertiary colors.”

Years later, while working with patients who had suffered damage to the temporal lobe, Khoshbin discovered that they perceive colors as being brighter and images as more vivid than people without the damage. “Sensory integration takes place in the temporal lobe,” Khoshbin says, “so it’s easy to understand how a disturbance in that part of the brain can create a different sensory experience.”

Khoshbin now believes van Gogh suffered from not just temporal lobe epilepsy, but also a personality disorder associated with it, dubbed the Geschwind syndrome. In the early 1970s, Geschwind had identified a constellation of five personality traits: hypergraphia, or voluminous output in writing or drawing; hyper-religiosity; unstable sexual behavior; intermittent aggressiveness; and clinginess.

Van Gogh exhibited all five traits. His hyper-religiosity, for example, once led to his being fired from his job as an evangelist minister for “excessive zeal.” He alternated between periods of hypersexuality and hyposexuality. His stormy relationship with the painter Paul Gauguin illustrated not only his clinginess—Gauguin bemoaned the difficulty of ending conversations with van Gogh—but also his aggression. It was just after threatening Gauguin with a razor that van Gogh famously lopped off part of his own earlobe and presented it with much flourish to a young woman.

Dramatic, too, was van Gogh’s hypergraphia. A largely self-taught artist who didn’t start painting until the age of 27, he nonetheless created more than 2,000 works of art before his suicide a decade later. The year he described the vibrancy of colors in the night sky—and painted his masterpiece The Starry Night—was so productive he was creating, on average, a new painting, watercolor, or drawing every 36 hours. When he wasn’t clutching a paintbrush or stick of charcoal, he was grasping a pen, writing long letters far into the night.

Those letters reveal much about van Gogh, from his obsession with color to his instincts for the divine.

“When I have a terrible need of—shall I say the word—religion,” van Gogh once wrote to his brother Theo, “then I go outside in the night to paint the stars.”

A Long Day’s Journey into Night

Without warning, one of Eugene O’Neill’s hands jerked, causing the 55-year-old playwright to splash coffee on himself. He then burst into a fit of weeping, the result not of the spill, he wrote, but of a “nervous impulse.”

By that time, O’Neill, winner of the Nobel Prize in Literature and already three of his four Pulitzer Prizes, had long suffered from an array of mysterious symptoms. His handwriting had become micrographic, his gait unsteady, his limbs uncoordinated, and his speech impaired. The impact on his life and art was debilitating.

Although O’Neill had been diagnosed with Parkinson’s disease a dozen years before his death at the age of 65, an autopsy performed by E. P. Richardson, Jr. ’43A revealed a more surprising neuropathology, one the physician kept confidential at the family’s request.

Decades later, Richardson and Bruce Price, an assistant professor of neurology and chief of neurology at McLean Hospital, secured permission from O’Neill’s surviving grandchildren to publish the postmortem findings. Their report appeared in a 2000 issue of The New England Journal of Medicine.

According to the report, O’Neill first noticed a tremor in his hands while a freshman at Princeton, but it did not affect his penmanship until he was 41. Two years later, he noted in his journal difficulty in controlling his pencil. His tremor continued to worsen, and by 1943, he had abandoned his journal because the physical process of writing had become torturous.

That same year, in response to a comment on the shrunken quality of his handwriting, O’Neill explained, “There is a physical reason for that—the curse of Parkinson’s disease—it’s easier to control tremor in minute writing.” But, he added, what most disturbed him more were the “fits of extreme melancholia that go with it. God knows I have had enough of Celtic Twilight in my makeup without needing any more of the same. And this isn’t the same. It isn’t sadness. It’s an exhausted, horrible apathy.”

O’Neill’s wife, Carlotta, described days when he could produce no more than a tremulous, illegible scrawl. “No one could read it but me,” she later recalled, “and I would type his manuscripts over and over for him. I nearly went blind.”

Neurological examinations disclosed poor articulation in O’Neill’s speech and hypotonia of his muscles. His head and torso would sway, even while he was seated. Although his gait was wide and foot placement erratic, his posture remained erect. He exhibited no symptoms of dementia.

Then, in 1952, O’Neill’s symptoms rapidly worsened. He had difficulty swallowing, became sullen and reclusive, and finally, a year later, contracted a fatal case of pneumonia.

The autopsy revealed that his substantia nigra—the brain region most affected by Parkinson’s disease—was unscathed. The playwright suffered not from Parkinson’s, Richardson concluded, but rather an idiopathic form of late-onset cerebellar atrophy, with extension into the anterior lobes of the cerebellum.

Although O’Neill himself and many of his biographers suspected that his early alcohol binging might have caused his neuropathology, the New England Journal of Medicine article argues strongly against it. When alcoholism results in cerebellar degeneration, poor nutrition and chronic alcohol abuse are at the root. In this case, however, the authors write that O’Neill’s personal records reflect an adequate diet and suggest he did not drink to excess for at least 25 years before his death and not at all during his last eight years. Other postmortem findings—including a normal liver and testes, organs frequently damaged by chronic alcoholism—strengthen the argument against alcoholism as a factor in O’Neill’s disease.

The report does not rule out a genetic etiology; the playwright’s family history hints at an essential tremor in his mother, a brother, and his older son. Yet the paucity and age of tissue specimens precluded DNA analysis.

Two decades before his death, O’Neill had embarked on a cycle of 11 plays intended as a critique of American civilization, which he viewed as caught between its professed democratic ideals and the greed that fueled its progress. Plagued by his worsening symptoms, he completed only two of those plays, A Touch of the Poet and More Stately Mansions.

In the year before he died, O’Neill burned the remaining unfinished manuscripts. His wife described the tragic scene: “He could only tear a few pages at a time, because of his tremor, so I helped him. We tore up all the manuscripts together, bit by bit. It took hours....It was awful. It was like tearing up children.”

Had O’Neill been able to fulfill his vision for that cycle of plays, Price says, “it might have become one of the most extraordinary works of American theater. Instead, his neurological illness stole his abilities and his life, depriving us all.”

This article appeared in the Harvard Medical Alumni Bulletin’s special report on history’s medical mysteries.