Brain-body medicine---what’s it all about?

I almost hate to mention brain-body medicine because, to a certain degree, the concept has been hijacked by quacks. The science of brain-body medicine is limited by inherent problems in methodology. Although the pseudoscientists have taken the concept beyond what this limited science can support, it’s worth looking at.

The Cleveland Clinic Journal of Medicine recently published the Proceedings of its Brain-Heart Summit. Cleveland Clinic’s heart-brain institute bears the name of Earl and Doris Bakken. Earl Bakken is the founder of Medtronic and is credited with development of the first wearable (a precursor to implantable) artificial pacemaker. Bakken co-authored the introduction.

Bakken also gave some opening remarks which, let’s hope, won’t define the focus of the brain-heart institute. Here are a few:

The mind is not in the brain. The mind is throughout the whole body and external to the body.

The sun and the moon have great impact on the function of parts of our body, including the heart and brain.

There are important roles for Ho`oponopono and naturopathic, homeopathic,
chiropractic, and blended medicine.


Energy medicine has an important role: reiki, chi gong, guided imagery, massage, taichi, yoga,healing touch, prayer, aloha.

(One has to wonder if Baaken, like Linus Pauling, is another example of a brilliant mind and humanitarian turned to the dark side).

But I digress. There was some good stuff presented.

Dr. Martin Samuels, Neurologist-in-Chief at Brigham and Women’s Hospital, reviewed the field of neurocardiology. The spectrum of neurocardiac conditions encompasses electrocardiographic abnormalities (e.g. cerebral T waves), segmental disease (takotsubo cardiomyopathy) and sudden death. The common denominator is catecholamine cardiotoxicity producing a characteristic histologic lesion known as contraction band necrosis, aka coagulative myocytolysis. This lesion is to be distinguished from coagulation necrosis which is the lesion of myocardial infarction.

The most dramatic example of neurocardiac toxicity is death following an intense emotional experience, sometimes termed “Voodoo death.” The degree of fright necessary to induce a fatal autonomic storm cannot ethically be induced in the laboratory, limiting researchers’ ability to test the model for neurocardiac death. Anecdotal evidence from antiquity to modern times, however, can be found in literature, anthropology research, medical journals and even the popular media (was neurocardiac toxicity the precipitating cause of Ken Lay’s death?). The evidence is compelling, and animal experiments coupled with observations of human cases, along with the help of some “experiments of nature” such as earthquakes and pheochromocytoma, have enabled scientists to better understand the neurocardiac pathway (which begins in the insular cortex) and gain some understanding of the biochemical mechanisms.

Some of the pioneering work on the model, as cited, for example, here, here, here, here, and here was done by Dr. Robert Eliot. His early interest in this problem was spurred by field observations on aerospace workers at NASA at the height of the space race. These engineers, who were under extreme occupational stress, suffered an increased rate of sudden cardiac death despite their youth and an absence of traditional cardiac risk factors. At autopsy contraction band necrosis was found much more frequently than coronary atherosclerosis. Eliot, who devoted much of his career to stress management as a means of reducing cardiovascular risk, was fond of saying “The brain talks to the body. The body talks back. Sometimes it’s a fatal conversation.”

Dr. Ilan S. Wittstein of the division of Cardiology at Johns Hopkins elaborated on one of the clinical forms of neurocardiac disease, takotsubo cardiomyopathy. This condition has, until recently, been mistaken for acute myocardial infarction and currently has several other names including stress cardiomyopathy, broken heart syndrome and transient LV apical ballooning. Patients most commonly present with chest pain and/or dyspnea following severe emotional stress. Pulmonary edema and cardiogenic shock may be present. Cardiac imaging reveals a peculiar apical wall motion abnormality which does not conform to a vascular territory. The name takotsubo derives from this characteristic pattern of apical ballooning despite preserved function of the basilar segments which gives the left ventricle the appearance of a takotsubo, a Japanese octopus trapping pot with a narrow neck. Although ECG changes which can be mistaken for ischemia as well as troponin leak often accompany the syndrome, myocardial ischemia is not the principal mechanism, with many patients being free of demonstrable coronary disease. Recovery in several weeks is the rule. Although there has been some controversy as to the mechanism of this syndrome, endomyocardial biopsies have revealed that the lesion is contraction band necrosis, thus warranting inclusion of takotsubo cardiomyopathy in the spectrum of neurocardiac disease.

Dr. Stephen Oppenheimer discussed in greater detail the role of the insular cortex in neurocardiac disease, noting that left insular strokes are associated with adverse cardiovascular outcomes.

This presentation deals with sudden unexpected death in epilepsy (SUDEP). Although some cases have a neurocardiac etiology, multiple mechanisms including neurogenic pulmonary edema and central apnea may be at play. It is worth remembering that cardiac channelopathies such as Brugada syndrome have been mistaken for epilepsy.

Dr. Cathy A. Sila discussed the strong association of heart failure and cognitive impairment due to multiple mechanisms. (AKA cardiac encephalopathy).

Brain-body medicine has biologic plausibility. But, because of the complex systems and unique methodologic issues that exist it is a popular form of quack fodder. In discussing this fascinating field we must be careful to make the difficult distinctions between science and pseudoscience.