Fran Lowry

March 02, 2011

March 2, 2011 (Los Angeles, California) — John M. Hallenbeck, MD, chief of the Stroke Branch at the National Institute of Neurological Disorders and Stroke (NINDS), has been given the Thomas Willis Award by the American Stroke Association (ASA).

The Willis Award, the ASA's highest honor, was presented to Dr. Hallenbeck at the association's International Stroke Conference 2011 in Los Angeles.

Dr. John M. Hallenbeck

The award is given for major contributions to the understanding of stroke "over a sustained period," according to the ASA. It is named for pioneer physician Thomas Willis (1621-1675), who is credited with providing the first detailed descriptions of the brainstem, cerebellum, and ventricles, along with hypotheses on their function. The circle of Willis was his discovery.

"This award recognizes the lifelong achievements of Dr Hallenbeck and his contributions to our understanding of stroke through his novel observations in animal models," said Ralph L. Sacco, MD, president of them American Heart Association and chair of neurology at University of Miami Miller School of Medicine in Florida. "His work on inflammatory and immune mechanisms in acute brain ischemia has led to potential future therapeutic approaches."

Paola Castri, MD, PhD, is a visiting fellow in Dr. Hallenbeck's laboratory at NINDS. She says of him, "Dr. Hallenbeck is not only an ardent physician-scientist, but he is also a great mentor, for he is thoughtful and incisive and continues to impart new ways of approaching scientific questions. I strongly believe his research on stroke mechanisms and therapeutics will be helpful to many people the world over."

Third-Generation Physician

Dr. Hallenbeck is a third-generation physician. His grandfather, Dorr F. Hallenbeck, lived on a farm as a boy and used to stay with a physician's family on his way to or from school when snowstorms in Minnesota made the 3-mile walk impossible and as a result was inspired to go into medicine, eventually joining the Mayo Clinic in Rochester.

His father, George A. Hallenbeck, also became a physician and was chairman of the Department of Surgery at the Mayo Clinic. There's a fourth-generation physician in the family, too. One of Dr. Hallenbeck's sons, Michael G. Hallenbeck, continues the tradition as a radiologist in California.

Young John went to medical school at the University of Pennsylvania. "I suppose there is a sort of programming that occurs with that kind of background," he told Medscape Medical News. "Medicine seemed like something that would be a good thing to do."

Dr. Hallenbeck did his residency in neurology at the University of Michigan. The Vietnam War was going on at the time, so Dr. Hallenbeck opted to take advantage of the Berry Plan, which allowed him to finish his residency before going into military service.

He was commissioned into the US Navy and assigned to the Naval Medical Research Institute in Bethesda, Maryland, where his research focused on central nervous system decompression sickness and air embolism. Later, he became interested in stroke, studying inflammatory and immune mechanisms in acute brain ischemia.

After 13 years of research, Dr. Hallenbeck was tapped to head the US Navy's neurology training program at the National Naval Medical Center. He also became professor, vice chairman, and chairman for research in the Department of Neurology at Uniformed Services University of the Health Sciences.

In 1991, he came to the National Institutes of Health, where he started the Stroke Branch.

From Decompression Sickness to Stroke

Currently, Dr. Hallenbeck's laboratory is studying the cellular regulation of ischemic tolerance and inflammatory and immune mechanisms that contribute to the initiation and progression of stroke. A focus of his work is on immunologic approaches to suppress the activation of endothelium that is caused by inflammatory cytokines, such as tumor necrosis factor and interleukin 1.

After receiving his award, Dr. Hallenbeck delivered the Willis Lecture entitled, "Tracks of a Nonmain Path Traveler." He chose that title, he says, because he was a no-main path traveler himself.

"Most people, when they go into an academic-level research career, would start out in someone's lab, where they would be taught the dogma about — in this case — stroke. And I came up very differently. I moved from decompression sickness into stroke," he told Medscape Medical News.

"By working on decompression sickness I was aware of the surface activity of bubbles in the blood that can denature proteins and can activate a lot of different systems in blood and tissues that can lead to inflammatory and immune responses. I carried all of this into stroke at a time when most people weren't thinking that way," he recalled.

"I felt from the beginning that, as blood flows through an injury zone in the brain, it is likely, because blood is very reactive, that it could be undergoing complex interactions with endothelium," he explained. "At the time, we knew only a fraction of what we now know that endothelium can do." Blood and endothelium do interact in a stroke, and that interaction can lead to inflammatory and immune changes.

The endothelium used to be thought of "as a sort of Teflon layer that kept the egg from sticking to the pan," but research in a number of laboratories during many years has shown that endothelium orchestrates hemostatic potential both locally and asynchronously through an organ, Dr. Hallenbeck noted. "The endothelium integrates signals that are coming from the blood but also from the vessel wall and from the surrounding parenchymal tissue," he said.

The properties of the luminal surface of the endothelium change according to the molecular signals that the endothelium is integrating, Dr. Hallenbeck continued. "It can become proinflammatory or procoagulant, but it's got to stay within a homeostatic range, otherwise you're in trouble."

But cycling back and forth between anti-inflammatory and anticoagulant states and proinflammatory and procoagulant states is the norm.

"This is happening all the time in all of us," he said. "In people with risk factors for stroke, however, the endothelial activation in brain vessels can exceed the homeostatic range and increase the risk for stroke. We are testing an approach that targets regulatory T cells that are specific for E-selectin (an adhesion molecule that is only expressed on activated endothelium) to activate blood vessels. This can suppress vessel activation and prevent strokes."

I'm in a field that is right for me. If I had tried to run a business or something, it would be ghastly.

Dr. Hallenbeck is content with the career path he chose — or was genetically programmed to pursue.

"Life is always better if you choose to do something that you can do fairly well, rather than to struggle with what you do or just be average at what you do," he said. "The other important thing is to be able to tell the difference. You need to know when you really like to do something and have some promise for that line of work. I'm happy with the choice I made. I'm in a field that is right for me. If I had tried to run a business or something, it would be ghastly."

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.

processing....