From the Archives: A Neuroscientist Describes His Stroke

At the AAAS/Dana event on sleep last month [see webcast], I was reminded of the time I interviewed sleep expert and Dana Alliance member J. Allan Hobson. At the time, he was excited about his Dreamstage Brain and Sleep Science Museum in East Burke, VT, and he also sold me on his book, From Angels to Neurones: Art and the New Science of Dreaming, which he allowed us to excerpt for a Cerebrum essay. Since then, we’ve talked with him about why we need to sleep to remember.

But his essay that hit me hardest was a more-personal one he wrote for Cerebrum in 2002, “Shock Waves: A Scientist Studies His Stroke.” Hobson had a stroke in 2001, and here describes his recovery in detail, trying to make sense of mysterious changes in his sleep and dreaming. Near-fatal heart failure, bizarre side effects of medications, and other aftershocks followed, and he kept trying to understand developments his doctors often dismissed. “A speculative theoretical bent has always characterized my science,” writes Hobson. “I feel impelled—and pleased—to turn it on myself.”

“Between my eighth and eleventh days, I had more dreamlike imagery during my fitful sleep, but none of the sort that commonly accompanies REM sleep.” (Image credit: © 2002 Ken Dubrowsk)

“Between my eighth and eleventh days, I had more dreamlike imagery during my fitful sleep, but none of the sort that commonly accompanies REM sleep.” (Image credit: © 2002 Ken Dubrowsk)

The essay is long and intriguing. I wonder how many of his observations have been confirmed or refuted in the dozen years since. Here’s an excerpt:

Time is exquisitely attenuated in the hospital because there is nothing to do except try to keep from drowning in my own saliva or falling off the bed due to vertigo. So I lay for hours in my bed, flat on my back with my eyes closed. The worst time is the night because I am alone, usually from 7 p.m. to 7 a.m., and because I cannot sleep a wink. The usual side position does not help; I’m just awake, my mind working actively in the dark all night long. Attempts to watch TV are frustrated by the banal programming and my double vision. Toward morning, at first around 3 o’clock and subsequently as late as 7, I suddenly feel irresistibly sleepy, but this is not normal sleep onset. Instead I am drawn into a hallucinatory visual world of great complexity, which only occasionally bears a faint semblance to real dreaming.

If sleep is totally suppressed, as was mine for the first 10 days, there of course can be no dreaming. During this acute post-stroke period, however, I did have abnormal visual experiences. During the whole 10-day period, I could visually perceive, immediately upon closing my eyes, a vault over my supine body, which resembled the bottom of a swimming pool, its surface aqua, white, or beige. Less often, it resembled engraved obsidian or a sort of gauze of ice or glass crystals. The most fully realized human images that I “perceived” were of my wife, featuring her lower body, and (most amusingly) of a Peter Pan-like version of a colleague, Robert Stickgold, and two fairies enjoying a bedtime story. Stickgold is a senior collaborator in my lab who does have a pixielike playfulness. While visual disturbances are not uncommon in Wallenberg’s syndrome, they have only been reported as occurring while awake and with the eyes open. Mine were behind closed eyes.

He continues on this theme later in the essay:

When researchers make a surgical lesion in the brain of an experimental animal, we almost certainly produce both primary effects (neuronal death) and secondary effects (neuronal dysfunction) of the kind that my stroke caused. As I mentioned when describing my early hospitalization, I knew that transection of a cat’s medulla at the mediopontine level produces an intense insomnia lasting about 10 days; normal sleep is recovered over the next 20 days. The more time that passes, the greater the recovery of function, the compensation for function, or both. We cannot know if this is simple recovery and compensation, which imply brain plasticity. But it seems probable, both from my own studies and from reports on other research, that the explanation of the insomnia is far less likely to be the disenabling of a supposed synchronizing mechanism in the lower brain than it is to be secondary damage to the areas of the brain adjacent to the primary lesion.

The moral: We must be cautious in drawing inferences about relationships between structure and function. Before concluding that a given sleep stage, with its associated mental experience, has been eliminated by a lesion, we need much longer observation than most experimenters have invested. We also need more searching psychological probes than neuropsychologists have used until now. When it comes to functions like dreaming, for which we rely on subjective reports, a subject’s ability to report may be intact—although, in my case, gross oversleeping during the rehabilitation proved an obstacle to dream recall and reports. Of course, we also need objective recordings to corroborate subjective reports. Did I really recover my REM sleep? Was it the same as my pre-stroke REM sleep? These are important questions.

–Nicky Penttila

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