There may be exaggerations or diminutions of depth and perspective or exaggerations of stereo vision—or even stereo hallucinations, seeing three-dimensional depth and solidity in a flat picture. Huxley described this:
I was handed a large colored reproduction of the well-known self-portrait by Cézanne—the head and shoulders of a man in a large straw hat, red-cheeked, red-lipped, with rich black whiskers and a dark unfriendly eye. It is a magnificent painting; but it was not as a painting that I now saw it. For the head promptly took on a third dimension and came to life as a small goblin-like man looking out through a window in the page before me.
The perceptual transformations and hallucinations induced by mescaline, LSD, and other hallucinogens are predominantly, but not exclusively, visual. There may be enhancements or distortions or hallucinations of taste and smell, touch and hearing, or there may be fusions of the senses—a sort of temporary synesthesia—“the smell of a low B flat, the sound of green,” as Breslaw put it. Such coalescences or associations (and their presumed neural basis) are creations of the moment. In this way they are quite different from true synesthesia, a congenital (and often familial) condition where there are fixed sensory equivalences that last a lifetime. With hallucinogens, time may appear to be distended or compressed. One may cease to perceive motion as continuous and see instead a series of static “snapshots,” as with a film run too slowly. Such stroboscopic or cinematic vision is a not uncommon effect of mescaline. Sudden accelerations, slowings, or freezings of movement are also common with more elementary hallucinatory patterns.34
I had done a great deal of reading, but had no experiences of my own with such drugs until 1953, when my childhood friend Eric Korn came up to Oxford. We read excitedly about Albert Hofmann’s discovery of LSD, and we ordered 50 micrograms of it from the manufacturer in Switzerland (it was still legal in the mid-1950s). Solemnly, even sacramentally, we divided it and took 25 micrograms each—not knowing what splendors or horrors awaited us—but, sadly, it had absolutely no effect on either of us. (We should have ordered 500 micrograms, not 50.)
By the time I qualified as a doctor, at the end of 1958, I knew I wanted to be a neurologist, to study how the brain embodies consciousness and self and to understand its amazing powers of perception, imagery, memory, and hallucination. A new orientation was entering neurology and psychiatry at that time; it was the opening of a neurochemical age, with a glimpse of the range of chemical agents, neurotransmitters, which allow nerve cells and different parts of the nervous system to communicate with one another. In the 1950s and 1960s, discoveries were coming from all directions, though it was far from clear how they fit together. It had been found, for instance, that the parkinsonian brain was low in dopamine, and that giving a dopamine precursor, L-dopa, could alleviate the symptoms of Parkinson’s disease, while tranquilizers, introduced in the early 1950s, could depress dopamine and cause a sort of chemical parkinsonism. For about a century, the staple medication for parkinsonism had been anticholinergic drugs. How did the dopamine and acetylcholine systems interact? Why did opiates—or cannabis—have such strong effects? Did the brain have special opiate receptors and make opioids of its own? Was there a similar mechanism for cannabis receptors and cannabinoids? Why was LSD so enormously potent? Were all its effects explicable in terms of altering the serotonin in the brain? What transmitter systems governed wake-sleep cycles, and what might be the neurochemical background of dreams or hallucinations?
Starting a neurology residency in 1962, I found the atmosphere heady with such questions. Neurochemistry was plainly “in,” and so—dangerously, seductively, especially in California, where I was studying—were the drugs themselves.
While Klüver had little idea of what the neural basis of his hallucinatory constants might be, rereading his book in the early 1960s was especially exciting to me in light of the groundbreaking experiments on visual perception that David Hubel and Torsten Wiesel were performing at the time, recording from neurons in the visual cortex in animals. They described neurons specialized for the detection of lines, orientations, edges, corners, etc., and these, it seemed to me, if stimulated by a drug or a migraine or a fever, might well produce just such geometrical hallucinations as Klüver had described.
But mescal hallucinations did not stop with geometrical designs. What was happening in the brain when one hallucinated more complex things: objects, places, figures, faces—let alone the
heaven and hell that Huxley had described? Did
