Monday, April 01, 2002

Shock Waves:

A Scientist Studies His Stroke

By: J. Allan HobsonM.D.

With an international reputation in dream research, Hobson met his toughest analytic challenge in February 2001: his own stroke. With his intellectual abilities intact, Hobson struggled to make sense of mysterious changes in his sleep and dreaming. It was just the beginning. As near-fatal heart failure, bizarre side effects of medications, and other aftershocks occurred, 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.”

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.