“Voodoo" Death A Look Into the Neurological Phenomenon
In this video, Martin A. Samuels, MD, MACP, FRCP, FANA, FAAN, DSc, discusses his presentation ‘“Voodoo” Death: A Window Into the Link Between Internal Medicine and Neurology,’” which was presented at Neurology Week. Samuels reviews the origins of "Voodoo" Death, a sudden death caused by shock or fear, along with modern advances in echocardiography.
Read the Transcript:
Martin Samuels, MD: Hello. I'm Martin Samuels. I'm a professor of neurology at Harvard Medical School. I'm the Marion Sidney Joseph Professor of Neurology at the Harvard Medical School, and I'm the Founding Chair Emeritus of the Department of Neurology at the Brigham and Women's Hospital in Boston.
Today, I'm going to tell you something about a very, very interesting phenomenon in neural medicine, that is the interface between neurological disease and internal medicine. That is the subject of what I have entitled "Voodoo Death."
Why have I given it this rather striking title? This is in honor of Walter B. Cannon, Walter Bradford Cannon, the great neurophysiologist, and Professor of Physiology at Harvard Medical School for an entire generation. He was the recipient of the knowledge of Ivan Pavlov, the great Russian neurophysiologist.
He met Ivan Pavlov in Boston in 1929 at the physiology meetings, where Ivan Pavlov, who was a generation older than Cannon, basically passed the baton to Walter Cannon as the greatest autonomic nervous system physiologist in the world.
Cannon was very interested in a phenomenon that he learned about from the anthropology literature, not from the medical literature, and that is what he called "Voodoo Death." This paper, which was written in 1941, was written as a summary of his life's work on this subject and is one of the most important papers we have in the field of neurological medicine.
What he meant by voodoo death was what we would now call frightened to death, that is, people who underwent a significant stressor of some sort. He would have said, "A life-threatening stressor with no chance of escape or control." He collected these cases from the world's literature in the anthropological journals.
Many of them were very striking. I don't have the time to tell you the details of all of them. These were cases in which a person was frightened by some powerful figure in their social group, and as a result of that, dropped dead. This idea has been known for a long time, but it was brought into the mainstream of neurological and physiological thinking by Walter Cannon's remarkable 1941 paper.
In fact, there is a story in the "Book of Acts" in the "Bible" about a couple named Ananias and Sapphira, who sell a possession, and as it says in the Bible, kept back part of the price. That is, they didn't pay the tax that they owed.
Peter the Apostle called Ananias before him and read him the riot act and said, "You've lied not only to man but to God." With that, it says that Ananias, hearing those words, dropped dead in front of St. Peter. That's remarkable in its own right, but there's more to the story.
The wife, Sapphira, not knowing what had happened, came in a few hours later. Peter said to her, "You've participated in this fraud, not paying your taxes. Your husband has been buried by those boys, who have taken the body out, and you're equally responsible," at which point she also dropped dead.
This is two cases of what Walter Cannon would have called voodoo death, sequentially. People have known about this for a long, long time, but it didn't have any scientific basis. The scientific basis was foreshadowed by the work of Ivan Pavlov on the autonomic nervous system and memory of autonomic functions that he did in his famous dog experiments.
The human work can be traced to a paper written by a man named Harold Levine, a very distinguished cardiologist from a family of cardiologists at the Peter van Brigham Hospital in Boston, which is one of the predecessors of my hospital, the Brigham and Women's Hospital.
Harold Levine wrote a paper in which he articulated that there was a group of disorders characterized by a change in the electrocardiogram which looked like a myocardial infarction but probably was not a myocardial infarction. In fact, it was something else. He called this non-specific ST and T-wave changes.
The year after Harold Levine's paper was written, George Burch and his colleagues at Tulane University in New Orleans and the Charity Hospital, named this phenomenon cerebral T waves, and that name stuck. To this day, almost every medical house officer knows what cerebral T waves mean.
They mean an abnormality in the electrocardiogram, often very dramatic, usually characterized by ST and T wave changes with deeply inverted T waves across the precordium and in the anterior leads, seen in a situation in which the patient has suffered some kind of a neurological injury.
That neurological injury can be structural, like a subarachnoid hemorrhage, or an intracerebral hemorrhage, or a head trauma, or it can be functional, by which I mean not structural, such as the frightened-to-death phenomenon that Walter Cannon called voodoo death.
What has been learned over the subsequent 50 years or so since these initial discoveries were made in human beings is that the lesion underlying this problem is different than the lesion of an ordinary myocardial infarction.
A myocardial infarction, as you all know, of course, is damage to cardiac tissue as a result of ischemia, usually because of a plaque rupture in a coronary occlusion. This lesion, it turns out, is not the same lesion as the one caused by cardiac ischemia because of coronary disease. That lesion pathologically is known as coagulation necrosis.
The lesion caused by stress, or structural lesions in the autonomic outflow from the brain, is something known as contraction band necrosis. Over the generations, this particular lesion has been given different names, but the current name that we use for this is contraction band necrosis.
The reason we use that term is that if you do a biopsy of the myocardium, which can be done in living people using an endocardial biopsy technique, one sees a pathological contracture of the cardiac muscle, indicating that this is not due to energy loss, as one would see in a coronary occlusion, but rather due to catecholamine excess.
These catecholamines, the adrenaline-like substances, are released to the heart from two different sources. One is via the bloodstream, coming originally from the adrenal gland. The other, more potent effect, is a direct release of catecholamines from autonomic terminals in the subendocardium of the heart.
It turns out that the distribution of those lesions in the heart is predictable in most cases, such that the beta-1 and beta-2 receptors are denser in certain parts of the heart than in others. In fact, at the apex of the heart, the beta-2 receptors are dominant.
Those have a negative inotropic effect. That is to say, the heart relaxes. At the base of the heart, they're usually dominant beta-1 receptors, which are positive inotropes, meaning that the heart over contracts.
About a generation ago, an eminent Japanese cardiologist noticed, using the newly developed technique of cardiac echocardiography, that some patients who have suffered an acute frightening event will develop chest pain, electrocardiographic change, an enzyme leak of troponin, as we measure it now, but don't have a myocardial infarction.
In fact, what they have is contraction band necrosis, and because of the distribution of the beta-1 and beta-2 receptors, the heart takes a characteristic shape that, to this Japanese investigator, looked like an octopus pot.
An octopus pot is the Japanese version of what we would call a lobster pot or a lobster trap. It has a large belly and a narrow neck. The fishermen put these pots down, as our fishermen put down our lobster pots, filled with bait. The octopus gets into the pot and then can't get out through the narrow neck. They pull that up, and they have octopus.
He thought it looked like an octopus pot, and so he called it the takotsubo, which is the Japanese word for the octopus pot, the Takotsubo-like cardiomyopathy, or acute catecholamine or stress-induced cardiomyopathy. This is a curious illness seen almost exclusively in post-menopausal women.
The reason for that epidemiology is still not known, as far as I'm concerned. It is a fact that about 80 percent of the patients will be post-menopausal women. They will have suffered an acute stressor, such as the loss of a close relative or a catastrophe, like this apartment building in Florida collapsing or 9/11, or anything of that order of magnitude.
Following that, the person gets chest pain, goes to an emergency department, has an abnormal electrocardiogram with changes in the ST segment and the T waves, has a troponin leak, indicating that this is a real cardiac injury, not just an electrical artifact of some sort.
If an echocardiogram is done, which these days is almost always done in these circumstances, it will show the left ventricular apical ballooning phenomenon that was called the Takotsubo-like cardiomyopathy.
The thing about Takotsubo-like cardiomyopathy is that it's a functional phenomenon, not a structural phenomenon. There is no coronary occlusion, so theoretically, these patients could recover completely and go back to normal. In fact, they usually do.
Unfortunately, during the period where the left ventricular apical ballooning is occurring, there is an increased tendency for malignant cardiac arrhythmias, such as ventricular tachycardia converting to ventricular fibrillation and other cardiac catastrophes, even including rupture of the left ventricle, which has been pathologically dilated.
Furthermore, we've learned that not all of these neurocardiac lesions produce the characteristic takotsubo-like shape. Some of them are mid-ventricular. Some of them are base disease of the heart. Some of them are just local dyskinetic ventricular wall, which in its own right can produce emboli, which go to the brain and other organs.
This is probably an under-recognized phenomenon, and it didn't exist in the medical literature until the Japanese investigator, a generation ago, saw this takotsubo shape using an echocardiogram. This is an example of a disorder which is characterized by what was a new diagnostic test, the echocardiogram. Ever since that was recognized, the number of cases has increased dramatically.
It's an underrepresented population. Many people have the misconception that when somebody has chest pain and a troponin leak in the context of an acute stressor, that they've had a myocardial infarction. In actual fact, though some of them may have had a myocardial infarction, many others do not have a myocardial infarction. They have a potentially reversible contraction band necrosis syndrome.
This, of course, has an effect on therapy because there are drugs that we can use, such as calcium channel entry blockers, beta blockers, alpha blockers, and free radical scavengers, which might interfere with the progressive necrotic disease known as contraction band necrosis.
We can pretreat people to avoid this phenomenon who have neurological catastrophes, such as a subarachnoid hemorrhage, which is a good example of the disorder of the central nervous system, which commonly produces this disorder in the heart.
This is an example or a window into the world of what used to be called psychosomatic medicine, what the Russian investigators called neurophysiological medicine, in which there is a disorder of the central or peripheral nervous system resulting in catecholamine excess, which results in secondary organ failure. We're probably looking at a disorder which is much more widespread.
We're looking at the tip of an iceberg, affecting other organs, such as the kidney and the skin and the bowel, but we don't have the electrocardiogram, a nice non-invasive test, in those organs to be able to find it. It's my view that this is an under recognized phenomenon, which causes, or can cause, permanent damage to the visceral organs if it isn't recognized promptly.
I hope, with this summary, you understand the concept of neurocardiac injury, the origin of the idea of so-called voodoo death or frightened to death, promulgated by Walter B. Cannon, and the modern science of echocardiography and the release of troponin as a result of a catecholamine mediated cardiac lesion. Thank you very much for your attention.
