Ellsworth (Buster) Alvord was a neuropathologist whose work and personality has inspired many neurologists during the past 6 decades. A native of Washington, DC, he received his Bachelor of Science from Haverford College in 1943, followed by a medical degree from Cornell University Medical College 3 years later. He then completed residency training in neurology and pathology at New York Hospital and Walter Reed Hospital. Dr Alvord later conducted neuroimmunology research at the National Institute of Neurological Disorders and Stroke in Washington, DC, before joining Baylor Medical College in Houston as faculty in neuropathology. In 1960, he became the Chief of Neuropathology at the University of Washington School of Medicine, where he continued to work and conduct research until his death.
Discoveries during the early part of his medical education must have inspired Dr Alvord's research career. It was shortly after Thomas Rivers, MD, developed the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis that a viral model of murine central nervous system disease caused by the neurotropic ribonucleic acid Theiler murine encephalomyelitis virus was first described. Both models were quickly recognized as having immunological and histopathological resemblance to multiple sclerosis, and both have since been used to study the underlying mechanisms of human inflammatory demyelinating disorders. It must have been an exciting time for an aspiring and hard-working neuroimmunologist.
The list of Dr Alvord's contributions to the field is impressive, and he had the ability to identify relevant research questions. In fact, many of the topics that caught his intellectual curiosity are again the focus of research for a new generation of investigators. In 1948, he published an article on the distribution of central nervous system autoantigen in EAE in the guinea pig. For the next 30 years, he mapped dominant determinants of myelin antigens in several species. He and his colleagues also identified the potential of myelin as a treatment of central nervous system autoimmune disease, an observation that was tested decades later in clinical studies. Together with other investigators from the Pacific Northwest (Don Paty, MD, included), Dr Alvord detected paraclinical disease activity in animals with EAE by magnetic resonance imaging in 1985. While he was one of the first to express caution regarding the limitations associated with the EAE model when studying multiple sclerosis, he was also one of the first to test antibodies against monospecific targets as therapy. In 1987, Dr Alvord and colleagues recognized the importance of age of infections in childhood in determining the risk of multiple sclerosis. In the same year, he studied the role of B cells in EAE, a cell type that had largely been ignored in this context.
In the last 2 decades of his life, Dr Alvord's research focused almost exclusively on gliomas, specifically on models that would allow the prediction of clinical and paraclinical outcomes. I suspect that this shift in scientific interest was mainly driven by the patients he was responsible for as a neuropathologist at the University of Washington. After the introduction of magnetic resonance imaging to clinical neurological practice, the requirements for frequent biopsies in patients with multiple sclerosis and related disorders no longer existed.
Teaching neuropathology to medical students, residents, and pathology fellows was another passion of Dr Alvord’s. A number of his former protégés became academic leaders in the field. Dr Alvord published on his teaching experience in neuropathology at the University of Washington in medical journals. He and his family have also been generous supporters of medical, scientific, and cultural causes in Seattle and other parts of the country.
I had the opportunity to be acquainted with Dr Alvord when I was a neurology resident at the University of Washington, and I can attest to the fact that he was an impressive man and physician. If I have one regret about my residency, it is that I should have spend more time with Dr Alvord and listened to his views on neuroinflammation and autoimmunity of the central nervous system. He will be greatly missed by many.
Correspondence: Dr Stüve, Neurology Section, Veterans Affairs North Texas Health Care System, Medical Service, 4500 S Lancaster Rd, Dallas, TX 75216 (olaf.stuve@utsouthwestern.edu).
Financial Disclosure: None reported.