Shock Waves: A Scientist Studies His Stroke

It was Saturday, February 2, 2001. My wife, Lia, and I were having breakfast at a café in Monte Carlo when I began quite suddenly to sweat and feel dizzy. The sweating was intense on the right side of my head. The vertigo—a sensation of the world spinning around me from left to right, and in a downward orbit to the right—was relieved by resting my head on the table or closing my eyes.

I assumed that I was suffering the effects of sleep lost on our overnight flight from Boston, and waited for the worst of my symptoms to subside. Then I walked with Lia back to the hotel. Reclining, I immediately felt better, slept for three hours, and had a light meal in the room. That night I slept fitfully, but in the morning I enjoyed a room service breakfast. As I pushed the food cart out into the hall, however, I had difficulty with my balance, which told me that my troubles were not over. In fact, they had only begun.By noon, 24 hours after the initial attack of sweating and vertigo, I was struggling to swallow. I had a huge flow of saliva in my mouth and throat; it felt as though I were drowning in my own secretions. My wife and I, both physicians, could not mistake or deny the signs. Vertigo, failure of muscular coordination, and now difficulty in swallowing with uncontrolled salivation pointed to an emerging stroke—and even to its probable location, my lateral medullary brain stem. Frankly, my wife had already suspected as much; she had put me on aspirin to prevent blood clots and on nicergoline, which dilates blood vessels, to increase blood flow.

In the emergency ward of Monaco’s Princess Grace Hospital an electrocardiogram showed atrial fibrillation, a heart rhythm often associated with stroke.

Assessing the Damage

The kind of stroke I had is called ischemic, in which a blood vessel is clogged by either a plaque in the vessel wall or a clot from elsewhere that lodges in the vessel. The other kind of stroke is hemorrhagic, in which the blood vessel wall tears and blood pours into the brain, causing extensive damage.

I was fortunate. I did not have a hemorrhage, and my stroke was confined to my lower brain stem, right above the point where the spinal cord enters the brain. Three magnetic resonance images (MRIs) revealed that my stroke involved a discrete area in the right lateral medulla (where the posterior inferior cerebellar artery distributes blood), centered on the right restiform body, the adjacent medullary tegmentum, and the overlying cerebellum.

If my stroke had been in my upper brain, where conscious experience, language, and volition seem to originate, I would have been far more likely to experience difficulties with cognitive function, such as the inability to perceive or execute language (aphasia) and to have long-lasting weakness, paralysis, or both, of the limbs on the side of my body opposite the stroke.

At Princess Grace Hospital, I had two formal neurological examinations, one on my third day and one on my tenth. They systematically catalogued the effects of the stroke, which together formed what is known as Wallenberg’s syndrome, the result of occlusion of the posterior inferior cerebellar artery:

• Movement difficulties (ataxia), most severe in my right leg but also affecting my right arm;
• Balance (vestibular) deficits and postural instability. Especially with my feet together and eyes closed, I tended to fall forward and to the right.
• Double vision (diplopia).
• Pupillary inequality, with the pupil of my right eye dilated more than my left;
• Loss of sensation, and sensations of burning and tickling, on the right side of my face;
• My lip drooping on the right;
• Paralysis of the muscles of my pharynx on the right;
• Paralysis of my right vocal cord;
• Mildly decreased sensitivity to pain and markedly decreased sensitivity to temperature change of the left side of my body below my neck.

A neurological consultant declared, “C’est classique”—I was a classic case. I confess that this depersonalization wounded my pride. Neither he nor any other doctor who saw me ever expressed any interest in what I was experiencing subjectively.

What they did was to keep refining the diagnosis. There was no indication of damage to cranial nerves XI (controlling movement of the shoulder and head) or XII (controlling tongue movement and sensation). An electroencephalogram (EEG) was normal; visual-field testing was unremarkable. An ultrasound study of the cerebral vascular systems revealed blockage of the right vertebral artery. Repeated EKG’s revealed persistent atrial fibrillation in my heart, which later would prove important, indeed.

My doctors started giving me anticoagulants to head off formation of further blood clots, but was my heart fibrillation the source of the clots? To check out that possibility, they attempted on the eighth day to obtain what is called a transesophageal EKG. They failed, however, because the drug they used to prepare me for the procedure made me psychotic. Convinced that I was being attacked by soldiers with fierce medieval weapons, I fought off the physician and his probe—anything but the docility the doctor had anticipated.

Sleepless, Dreamless, and Hallucinating

In the first 10 days of my hospitalization, I had the predictable manifestations of Wallenberg’s syndrome, already described, which are readily found in any medical textbook and well known to doctors. But I also had other experiences, including total insomnia—a symptom not previously reported in the neurological literature. I knew that my brain lesion was precisely localized, and realized that my own sleep suppression closely resembled the insomnia that I had observed in cats who, as part of my research on sleep and dreaming, had undergone experimental brain-stem changes. I became determined to describe the subjective effects I was experiencing that were outside the parameters of my “classic case.” On the sixth day, February 8, I dictated this note to Lia:

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.

The severe suppression of my sleep continued for about two weeks, although I obtained some relief through antihistamines, which I was given starting on the eighth day. On February 15, two weeks after the stroke, I wrote: “Among the strange psychic phenomena is the continued sense that normal sleep and dreaming are impossible. Last night I had the image of the antihistamines working on anterior hypothalamic sleep mechanisms, but my lower brain-stem sleep system could not be definitively turned over.”

During this period I also had hallucinatory experiences involving balance—vivid impressions of being launched through space. These never accompanied the visual hallucinations that I just described; they came with their own imagery, which could be brought on by moving when I was awake during the day or could occur spontaneously at night as I lay in bed trying to sleep. The first, and most violent, was on my first night in the hospital. Here is the journal account I made the next morning after vomiting my breakfast:

I suddenly felt as if the bed were rotated 90 degrees in a counterclockwise direction and catapulted downward toward the front of the hospital and into the sea. The illusion that I was actually moving at very high speed for at least 100 meters through space was so completely convincing—and so terrifying—that I said to myself, “So this is what death is like.” To my amazement, these sensations abated as rapidly as they had begun, but they made a very lasting impression on me.

On First-Person Reports

What I give here is a subjective report—always suspect scientifically. Sleep science has learned to deal with such reports, however, in part by correlating specific aspects

of a patient’s description with whatever anatomical and physiological data are available. This approach could be compelling and informative in connection with strokes, as well, if scientists could overcome their natural misgivings about subjective data. One key would be to record the subjective experiences of stroke victims more aggressively, thoroughly, and systematically.

How? Well, neurologists need to be sensitive to the significance for research of these subjective experiences and to develop techniques for obtaining information on them. As in my case, family members are almost always willing and able to help. Inexpensive handheld tape recorders can augment reports dictated to others.

Without such proactive steps, a patient is reduced to a set of readily localizable signs of central nervous system damage; he becomes just another “classic case.” It surprises me that Adolf Wallenberg himself did not inquire about sleep and dreaming when he first described the syndrome in 1895; he was respected as a thorough clinician. Yet, in 50-odd papers describing cases like mine, I find not a single mention of the phenomena I describe: initial severe insomnia, suppression of dreaming, gradual and incomplete recovery of sleep, recovery of dreaming, and subsequent oversleeping. The sole first-person account that I did find of the effects of lateral medullary infarction, the kind of stroke I had, makes no mention of any change in sleep or dreaming.

Beginning to Dream Again

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: dreaming with elaborate and rapidly evolving plot, movement, bizarreness, dynamic emotion, and so forth. Here are two descriptions of my dream imagery on day 8:

I have the sensation of having paper all over my body which cannot be removed because there is a computer program that instantiates equal and opposite commands each time I try to remove one of them. This fruitless struggle goes on for hours and gradually replaces the alternating state of lucid thinking and lush visual hallucinations of the preceding 6 nights.

I see a female monkey whose head and paws are made out of silver foil containing brown flower petals. The monkey mama is floating in the air in front of me like a comical beatific protector.

On the 10th day, my dreaming for the first time involved a human being and the beginnings of a dreamlike narrative structure:

Ed Schott, one of my coworkers in Boston, is filling in brain drawings for people who want to know how the brain works and he has made a huge quilt out of about thirty or forty drawings, all of which were in color and connected together in a scrupulous way. I said, “Look, Ed, you don’t need to do all this for the other people, why don’t you keep this one for us and just send them a copy.”

Fragments like these were similar in form to my REM dreams before the stroke, but were not sustained. My typical REM-sleep dreaming did not return for exactly a month. By that time, I had been flown back to Boston by air ambulance and was in Brigham and Women’s Hospital. On the 31st day following my stroke, I had this experience:

Before I woke up I had a prolonged and interesting dream experience, in which I imagined that I was being treated by a woman or two women (possibly nurses) who were giving me magical fabric to put on my skin. This fabric released a kind of coolness and pleasurable sensation over my skin which I relished and I kept enjoying it as the fabric was moved from place to place on my hands, my chest, my belly, and my face. It was a little bit like the coolness that emanates from the ice packs that I used in waking to counter facial paresthesias, but very gentle and not like any other sensation that I have ever experienced. Nor was this dream like any other I ever had, because it just continued on and on and on in this wonderful analgesic, almost narcotically pleasant mode.

I remember wondering what the mechanism of the cool pleasure was and being unable to come up with any reasonable explanation. I knew that I couldn’t reason well, but even this recognition still didn’t lead me to think that I was dreaming. Instead, I attributed it to warmth of women who had obviously made an important discovery on how to comfort people. I would guess this went on for about 30 or 40 minutes until I gradually woke up, and then I could go back and forth for about five minutes in and out of this dreamy state. But by five o’clock in the morning I was too wide awake to do anything else but remember it well, contemplate it, and vow to tape record its contents.

Although it was nothing like any REM-sleep dream I had ever had, I hoped the dream meant my spontaneous sleep mechanisms were recovering. My first elaborate, sustained dream did not occur until Day 38, after I transferred to Spaulding Rehabilitation Hospital and began to walk and exercise. Here is what I wrote about the dream:

It took place in a foreign country, which I thought might be Yugoslavia or Hungary. Lia and I were on a trip, and we were crossing a bridge with a lot of other people. It was a high arched bridge of a medieval sort. The bridge suddenly separated from the land and became a boat skimming across a very small river to get to a village on the other side. We had plans to stay in an old-fashioned inn.

There was already some discomfort and difficulty finding each other as we got the boat near to the shore. I caught glimpses of her. She was talking to someone else, a man. At one point, either before or just after we got off the boat, I noticed that she had given or sold to him a half-inch bit used with my large brace to drill holes in wood in Vermont. I was very surprised and somewhat hurt by this. I noticed also that the bit had been used to make a very perfect hole in the shoulder bag, which the man wore. It was a shoulder bag very much like mine.

In the dream, Lia explained to me that she had sold the drill but would give me the money. It still seemed to me odd that she would give a stranger one of my most precious tools without asking me. I was feeling very vexed and apprehensive. We got on the land, we walked around looking for the inn, and we were separated from each other on several occasions. During one of the times that we were together, she made it clear to me that she needed to have a secret life.

When I was asking her about this man, it was clear that she meant that she needed to be free to have an affair with him if she wanted to. I found that very odd and very disquieting and tried to express my concerns. When we finally got to what appeared to be the inn, there was a strange scene in which she was again difficult to find. But I found her in what looked like a kitchen, and she was preparing to cook some food, which struck me as odd, since this was such a flimsy excuse. I asked her when she would be finished, and she looked at her watch and she said 45 minutes, to which I agreed, knowing that this was all the time she would need to make love with whichever stranger she had selected.

I then walked around the inn, which had a very peculiar structure. On one side, there was a row of seats roofed over as in a theater and beside each of the seats were exotic bouquets of flowers. I walked down from one level of this improbable architecture to the next, finally getting to the bottom, and wondering in which room Lia and her lover were situated and how I could get to the window to see it. But by going down, I was of course going down from the bedroom level, as if to avoid my curiosity. I wandered all the way around the other side of the building, admiring the ancient medieval architecture, all of which was quite exotic and entirely impossible. When I came back to the place where I thought I might find Lia, there indeed was her coat, the brown coat with the fur trim and hood that she wears so often and that I like so much, but no sign of her and no sign of whatever man she might be with.

Here was a REM-sleep dream if I ever had one. What makes that so likely is the 603 words in the description; researchers have found that reports on dreams occurring during non-REM sleep are typically less than 100 words. Nor must you be a psychoanalyst to discern the dream’s meaning. Cognizant of the damage inflicted on me by the stroke, I was feeling vulnerable to rejection by the woman I loved, the most important person in my life. I have often argued that the meaning of dreams is commonly transparent; this was a good example.

Brain Damage, Natural and Experimental

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.

The only aspects of my consciousness that needed to be rehabilitated after my stroke were the comfort of sleep and the experience of dreaming. My reports substantiate that my cognitive functions were not only intact but extended: After all, I spent far more time awake than normal—noticing, recording, and analyzing my mental and physical states.

Before I left Monaco, two women friends traveled all the way from Bordeaux to visit me. This expression of love buoyed my spirits. My survival and recovery were enhanced enormously by the support of a far-flung social network. Via e-mail, telephone, fax, and airmail, I was in touch with colleagues and friends from around the world and from earlier epochs of my life. This communication continues to enrich me, and I hope that this account may put me in touch with still more people who know my work or have shared some of these experiences.

As my brain healed (or perhaps just settled down), I slept better—at times too much, slowing my efforts to relearn how to walk. This prompted my doctor at Spaulding Rehabilitation Hospital to put me on Ritalin as a stimulant, although I mightily resisted the suggestion out of fear of becoming addicted. After a month of painful daily practice, I could walk with a cane and go home to my family. Shortly thereafter, I threw away the cane. On April 16, I was home, in my own garden, happily celebrating the fifth birthday of my twin sons.

Second Wave

In the months following my discharge from Spaulding, I reclaimed my life and enjoyed a wonderful summer. I gloried in resuming an almost full range of activities, traveling to Sicily with Lia on June 16 to spend the summer in our apartment in Messina. This included, in late June and early July, a beautiful vacation in Stromboli.

In Messina, I completed a first draft of A Short Introduction to Dreaming for Oxford University Press. It was fun to write, but above all reassuring to show that I could function as I always had, writing in the morning in my office in Messina or on the dining porch at the Hotel Miramare in Stromboli. I even made a good start on Experimental Animal, a book about my life and my dreams. Lia and I enjoyed social activities, including dinners and long weekends with friends. Adding to the excitement, we had the opportunity to hear Bob Dylan in concert in Taormina. All in all, I felt extraordinarily positive about my future, and utterly unprepared for what autumn would bring.

Not that all my symptoms had vanished. In Messina, I tried to wean myself off the 20 mg daily dose of Ritalin I had been taking since early April, but I simply could not make the cut from 10 to 5 mg without my motor system reacting. I was almost incapable of initiating movement until I went back to up 20 mg. The telephone in our hallway would ring four times before I could struggle out of my chair.

In retrospect, it may have been wise to trust my instinct to resist going on Ritalin in the first place. I wonder if my cardiovascular and cardiopulmonary motor system became dependent on this externally applied dopamine-like agent. On the other hand, perhaps my withdrawal from the drug was not gradual enough. In two attempts, I spent four days at each drug level—20, 15, 10, 5, then 0—as I withdrew. Thus complete withdrawal occurred in four steps over two weeks. The second time I had no particular difficulty, so it is unclear what contribution Ritalin or withdrawal from it made to the events that followed.

Crash

On a Friday in October, eight months after my initial stroke in Monte Carlo, I drove my sons, Andy and Matty, to Vermont. Lia was still in Europe. We left early in the morning, when I normally would feel perfectly refreshed. Instead, I was so drowsy that I stopped at least three times to keep from driving off the road. I assumed this was a hangover from Ritalin withdrawal.

Arriving in Vermont, I hooked up with a friend, Nick Tranquillo, and spent a lovely Friday afternoon and evening with him. I enjoyed Saturday, too, as friends from Boston joined us. This was the legendary Columbus Day weekend retreat of the Harvard Laboratory of Neurophysiology staff, which had been canceled for two years owing to the death of Lia’s parents. For me, the gala was particularly exciting because I felt that I had been granted a second life. Work was going well at the lab and the Vermont foliage was glorious.

One of my schemes for the weekend had been to dragoon visitors into picking up small branches from wood lots that had recently been cleared. But when I walked across the fields to check things out, I was aware of feeling not just tired, but tired in a specifically cardiac sense. Something about fatigue is distinctive when the heart is the culprit. You know that your cardiovascular system just won’t deliver the energy to move. I only felt better sitting on the ground, not moving. I quickly abandoned the woods project, knowing I wouldn’t be able to supervise it, much less participate. I dragged myself back to the house, determined at least to be a jovial host.

That was easy. My guests were delightful, and people kept arriving until a total of 17 sat down for a splendid dinner on Saturday night. I felt giddy and wonderful, not a bit tired. I did have a cough, but no fever, malaise, chills, or other signs of being ill. After dinner, I went to bed but slept poorly and the next day, for the first time in my life, didn’t want to get out of bed. Venturing downstairs, I saw that no one else was up. I went back to bed and stayed there most of the day. I ate no breakfast, fixed my guests a lobster bisque for lunch but ate only a token amount, and skipped dinner.

By then, I admitted to myself that I was sick, but didn’t know with what. Monday, I was so weak that I asked Ed Schott to drive me back to Boston. When we got there, he called my doctor, Jamie Winshall, who told me to go to Brigham and Women’s Hospital by ambulance the next morning. We then telephoned Lia, who began a hasty return from Sicily.

Intensive Care

On Tuesday, October 9, an ambulance took me to the emergency ward at the Brigham. When a chest x-ray revealed that at least three lobes of my lungs were infiltrated with pneumonia, I was put on massive doses of intravenous antibiotics.

Because it is not isolated in a single lobe, this type of pneumonia is called “atypical.” It doesn’t come on quickly or give you the chills, fever, and intense sense of illness that typical pneumonias do, but it was nonetheless malicious—probably caused by many episodes of breathing food into my lungs as, over the summer and fall, my dietary indiscretions had multiplied. I didn’t like being in the hospital, but two days on antibiotics made me feel better. I hoped to be discharged in a week to resume my life.

Instead, on Thursday night, October 11, apparently while asleep, I suffered acute cardiovascular collapse, with blood pressure readings of 60/0. I did not respond to attempts to rouse me. The hospital immediately put me in the intensive care unit, where for five days I lay near death.

I have no memory of those five days, but am told I was conscious much of the time. According to Dr. Winshall, I may have had an acute “aspiration event”—breathing food or fluids into my lungs—or perhaps the acute toxic state of the pneumonia precipitated this major setback. I accept neither of these theories. I will discuss my own hypotheses later.

Bizarre Psychological Experiences

From this point on during my hospitalization I suffered from the same insomnia that I had experienced during the original post-stroke period in Monaco: total, wall-to-wall, bolt-upright waking through the entire night. This drove me to seek relief through various sedatives, but I found little. Instead, I experienced bizarre psychological side effects.

Taking these drugs provided a series of natural experiments, visited on me by unwelcome circumstances, but which I knew how to exploit. Writing my book The Dream Drugstore (MIT Press, 2000) over the past two years had led me to ask myself why, given my intense, lifelong interest in dreaming and hallucinatory experiences, I had never taken psychedelic drugs. My honest answer: fear. Now that I had an opportunity to take them for valid medical reasons, I was astonished at the range and intensity of effects.

Serax (oxazepam) is a short-acting benzodiazepine with sedative hypnotic properties. Over the years, I had prescribed it for patients without knowing the effects it might have on consciousness. In me, Serax induced a sleepy state with confusion and an extraordinarily disturbing symptom. Thinking myself awake, I would reach for a glass on the bedside table—only to find that it did not exist. My hand would pass right through it. The same unnerving insubstantiality characterized many other objects. This must have resulted from my hallucinatory construction of an unreal glass, but I do not have a clue about what causes this disturbing effect, which was neither normal sleep nor normal waking, but a hybrid state with elements of both. I was in a robust mini-delirium.

Ambien (loroazpam) is associated with confusional states in the elderly, and it certainly confused me. I took it twice and both times had similar reactions: I was convinced that I was sleeping not in the hospital but in an attractively designed summer camp. There were families there that I might or might not know, but I sensed that I should know them. There were women talking, in what I took to be a kitchen, about making provisions for the other campers. Later, I realized that these were the voices of nurses outside the door of my hospital room.

During these long episodes on Ambien, my sleeplike transformation of consciousness was almost euphoric. Far from being in a hospital bed, I was atop a huge pile of mattresses, perhaps rolled and stacked on end, but very soft. I could sink down in them to any level, then have my consciousness follow me through these lovely, deep folds. Reality, of course, was my plain hospital bed, but it didn’t feel that way. My conviction that this was a very special camp was total. It was pleasant and reassuring to hear the women talking outside my door, in part because many spoke in accents that sounded Latin, as does Lia. Many of the nurses were Latinas.

“In the intensive care unit, sooner or later everyone becomes psychotic,” said Dr. Lowenfeld, its director, after my initial episode of delirium. I had begun to reexperience hallucinations at the onset of sleep, but here I want to describe the more distinctive effects of yet another drug, Benadryl.

On Wednesday, the night after my recovery from shock and respiratory failure, I had been sleepless despite taking trazadone and oral Ambien. On Thursday night, Bob, my nurse, reminded me that I should not be taking medication orally. He suggested sedating me with morphine through the intravenous line in my arm. Seeing this as an opportunity to describe the subjective experience of narcotics, I readily assented, but the morphine had no effect whatsoever on my perceptions—or my sleep. Even a second 25-mg dose left me awake and lucid.

Bob then suggested an antihistamine, Benadryl, a popular over-the-counter drug used for years as a clinical sedative. Here was a good chance to test a theory. Blocking histamines in my cortex ought to produce a dreamlike experience; indeed, my colleague Clifford Saper had identified the specific arrest of histaminergic neurons in REM sleep. His report put histamine cells in the same category as the serotonin- and norepinephrine-containing cells that turn off REM cells, a discovery I and my colleagues had made 25 years ago. We had also suggested that the specific features of dream consciousness were invoked by the demodulation of the cortex. By taking Benadryl, an antihistamine, I might thus learn more about the sudden, acute impact on perception of blocking my histaminergic cortical-activating system.

Admittedly, this was a messy experiment. My inferences about the drug’s mechanisms are tainted by what researchers would call the dirty chemical conditions of the experiment, not least my prior doses of morphine. But the effects of the Benadryl were so striking and specific that I note them here.

One advantage of administering Benadryl intravenously is that the subject has immediate awareness of the drug entering his circulatory system; it feels as though the injected vein is warming. No sooner had my right anticubital vein begun to heat up than there appeared the first in a succession of images on the ceiling over my bed. They were computer-animated sketches of imaginary reptiles, a show that came complete with the catchy title “Thalamo-Saurus” rendered in elaborate artistic computer graphics. Four characteristic reptiles trundled past in a specific sequence. The one I recall best was a blue-and-red crocodile, but a green-and-yellow lizard typically followed him. There were at times butterflies, birds, and fish. With my eyes open (and only then), these images would muster up on the right side of the ceiling over my bed, and then, as I watched in wonderment, march diagonally to behind my head on my left. I realized that I was having visual hallucinations.

By and large, these hallucinatory reptiles were friendly. I enjoyed them, especially when I realized that I could alter their speed and location by making eye and head movements. Otherwise, however, their trajectory was consistent, their appearance repetitive and clear, and their artistic characteristics harmonious and even beautiful. Amazingly, there was even a credit for the studio in Tokyo that had made this show. The show’s apt and imaginative title, “Thalamo-Saurus,” suggests imaginary reptiles conjured up by my drug-soaked thalamus.

Hallucinating in the MRI

I also developed a new case of double vision, and when I reported it to the neurologists, they suspected an extension of my lateral medullary infarct and sent me to the brain-imaging unit for another MRI. The results were reassuring—no evidence of spread. Still, I remain convinced that my stroke-related functioning has been worse since the ICU episode.

The MRI itself, though, was unnerving. It was my third. The first two, in Monaco, were equally stressful, but without the psychotic effects I experienced during the one at Brigham, where I became convinced that a young child and his mother were with me inside the MRI magnet chamber.

At one point, my hallucinatory perception of voices convinced me that many people, all standing up, were in the magnet chamber. As a physician, I know that MRIs focus on one and only one subject’s brain at a time. Obviously, I was that subject and I was lying down, but my brain easily tipped into delirium, probably because I was still suffering from a reduced supply of oxygen to my tissues, was still under the influence of drugs, and was sensorially isolated in the magnet.

From Damaged Brain to Disordered Mind

My subjective experiences in Monaco most probably resulted directly from damage to my brain stem. The impact on my functioning was, however, far more extensive than what might be expected just from the lesion visible on the MRI. I do not think, for example, that the initial suppression of sleep and dreaming can be ascribed solely to the lesion. Adjacent structures in my brain must have been dysfunctional, at least temporarily.

If I am right, consider the importance of this logic for all our lesion studies of sleep, including some of the most basic sleep research work. The infarction (which is the lesion) killed neurons in many parts of my brain: the restiform body, the cerebellum, the vestibular nucleus, the trigeminal nucleus, the glossopharyngeal nucleus, the vagus nucleus, and the nucleus ambiguous. This damage can be clearly associated with my acute post-stroke symptoms: vertigo, sweating, ataxia, my still unsteady and broad-based gait, excess salivation, and dysphagia (difficulty swallowing). Moreover, this damage is permanent, and thus responsible for the residual symptoms: ataxia, hypersalivation, dysphagia, facial anesthesia and paresthesia, and insensitivity to pain and temperature change on the side of the face opposite the stroke.

But—and this is the crucial point—these lesioned structures alone probably are not responsible for the sleep loss, suppression of dreaming, and visual hallucinations. It is more likely that these effects resulted in part from temporary functional deficits in another, unlesioned part of my brain, the pontomedullary reticular formation. This structure was clearly impaired during the acute post-stroke period. My double vision, for example, suggests malfunctioning of the oculomotor and preocular pontomedullary reticular neurons. Once these structures adjacent to the actual stroke lesion had regained their functional integrity, my sleep and dreaming recovered.

The Brain-Heart Sequence

My attack of pulmonary and cardiovascular dysfunction in October was discrete and different from anything that I experienced before it. Nevertheless, it came within a sequence continuous with my stroke. Can we mount an argument that the sequence was, in fact, a causal chain?

In the two weeks between September 15 and October 5, I developed, simultaneously and in parallel, both severe pulmonary infection and heart failure. The pneumonia may have been incubating for a long time, as frequent small episodes of breathing food into my lungs set the stage for it. This would be understandable; I had been eating with relish since early that July, regaining all of my pre-stroke weight of 200 pounds, an addition of 35 pounds in six months.

At the same time, my cardiovascular function was racing downhill. This is more puzzling. Could it be related to my worsening pulmonary function over two months as a result of coughing and regurgitating food? Was I fomenting an infection of both heart and lungs—or were both systems dysfunctional as a result of my brain stem lesion?

Two weeks before I was hospitalized at the Brigham, I noticed that I could not finish mowing my lawn; but I interpreted this as fatigue associated with reducing my Ritalin dose. Admittedly, my development of cardiovascular symptoms did come right on the heels of my forced weaning from Ritalin. It is ironic to imagine that this weaning, strongly urged in the interests of my heart, might actually have contributed to my heart failure. Whatever the cause, though, I rapidly was becoming a cardiovascular invalid. Then came the day in Vermont when I found myself unable to walk across the fields.

The most conservative scientific account of my three problems is that they are unrelated, purely coincidental: I have one tendency to stroke, another to pneumonia, and a third to heart disease. Frankly, I favor an alternative model: the problems of all three systems are causally interconnected. Here is how that might work.

The initiating episode is the thrombus, or clot, in my vertebral artery. This causes partial blockage of the posterior inferior cerebellar artery and launches my stroke. Fully 24 hours later, the deprivation of oxygen and nutrients—anoxia—has destroyed many structures in the lateral medullary and pontine tegmentum region on the right side of my brain stem. The damaged structures are parts of the oculomotor system, the trigeminal sensory system, and the seventh nerve enervation of the face. More specifically, and more severely, there is damage to vestibular, cerebellar, glossopharyngeal, and vagal neurons—all known to be associated with autonomic control of the brain, lungs, heart, and other viscera. The vagal nerve, when stimulated, is a major source of input to the heart, slowing it dramatically.

The next point in this causal sequence is that I have a problem with cardiac rhythm and rate—my heart beats too irregularly and too rapidly to be efficient. Why? The doctors call it idiopathic (“We don’t know why.”) and decline to speculate, but I do not. To the extent that cell loss occurred in the pons in my brain stem, many of my norepinephrine-containing neurons might have been killed along with sensorimotor neurons. This would set the stage for failure of the autonomic systems that supply nerves not only to the brain itself, but also to the heart and lungs.

How precise can we be about causes of the cardiovascular effects that I experienced? From the start, it was clear that autonomic functions controlled by the right vagus nerve may have been impaired. The vagus nerve also contributes to the control of secretion from the salivary glands and stomach. Specifically, it contributes to the way these secretions are moved up and out of the lungs and then down to the gastrointestinal tract. It may be that the severe disruption of this transoropharyngeal traffic led to my pneumonia. But the vagus nerve serves more than the pulmonary system; it has powerful slowing effects on the heart.

Now my hypothesis: The irregular heart action first seen in the emergency ward in Monaco was caused by my stroke, not the cause of it, as most of my doctors believed. The cause of my stroke was a blockage in a small artery supply blood to my brainstem. When that blockage occurred (and I felt dizzy), many of the brain cells controlling my heart rhythm were killed or so badly damaged that they no longer could control my heart, which thereafter beat rapidly and irregularly. It still does, although the rate is held down by medication.

Deprived of rate control, my heart beats insufficiently; it pumps too little blood to support my body’s functions, especially my leg muscles. Over time, my heart muscles also have been weakened by the lack of substance usually supplied by the heart slowing/heart speeding-up brain cells that were destroyed. That is why I am always weak and tired. I am sitting on the edge of heart failure.

Making Sense

A speculative theoretical bent has always characterized my science. I feel impelled—and pleased—to turn it on myself, Allan Hobson the patient. Integrating my wild concatenation of symptoms into a model rooted in my life’s work is intellectually gratifying—and quite possibly therapeutic. As preliminary and perhaps fanciful as that integrated model may be, I prefer it to no model at all.

Today, I am far from the physically hearty, athletic, and emotionally charged man I was before my stroke. I walk with a wobble. I cough explosively. I feel a constant tugging of my right eye and cheek. I have an unnerving sensation that someone is giving me a hotfoot in my left shoe. Yet, the part of me that is healthy can observe, analyze, and hypothesize about the part that is ill or dysfunctional. At first, when people would ask me how I was doing, I would hesitate, then offer either of two useful stories: 1. I am fine, or 2. I am very impaired. Now I say, “The part of me that is talking to you is fine.” That says it all.

Author’s note: I have published a more technical account of my experiences in the scientific journal Consciousness and Cognition.