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Monday, April 01, 2002  Shock Waves:   A Scientist Studies His Stroke  By: J. Allan HobsonM.D. [continued]

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. 

Lying in the dark, still and quiet, as MRI images are being collected is a special case of sensory isolation. After about 30 minutes of hearing the magnet whining and cranking, I was ready to get out, but a technician’s voice several times admonished me, “Please don’t move, the session is almost over”—before admitting that I still had 10 minutes to go. By then, I was sure that the young boy, who was whimpering, and his mother, who was reassuring him, were suffering even more than I. I reached out to them, reassuring them that our torture would end soon and we would emerge unharmed. 

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. 

Can we go further, speculating on details of the underlying mechanics of these effects? With regard to the visual hallucinations, I can offer only a provisional model of explanation. Whenever the balance of our neuromodulatory systems is upset, whether by sleep deprivation, therapeutic drugs, drugs of abuse, or organic insult to the brain, the result can be visual hallucinations. This means that the brain-mind is capable of producing formed visual imagery not only without external sensory input (as it does in dreaming) but simply by tuning out external inputs (just closing my eyes set all that reptilian imagery in motion), thereby altering the balance between external and internal stimuli. 

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. 

It is plausible that impairments to my vagus and glossopharyngeal nerves could lead to a secondary impairment of pulmonary regulation. The ability to clear the lungs of fluid would then be compromised, and the propensity toward pneumonia increased, not only because of the swallowing defects but also because of a weakening of the defensive reactions to aspiration. This could explain the pooling of fluid and excessive secretions of mucus. This process, in turn, could causally tie in to my stroke and pneumonia.

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.