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By Joel A. Vilensky

In his recently published book, Britain and the 1918-19 Influenza Pandemic: A Dark Epilogue (Routledge, 2006), Niall Johnson states unequivocally that encephalitis lethargica (EL) was related to the influenza pandemic of 1918. Although other authors have also advocated such a view, and despite the fact that the two diseases occurred approximately contemporaneously, the general consensus among neurologists is that the two diseases were probably unrelated.

Accordingly, there were significant differences between influenza and EL in characteristics with the most notable being that whereas influenza was highly contagious, EL was not. Similarly, only a minority of EL patients reported being previously ill with influenza. Furthermore, probably the strongest evidence against an influenza cause for EL is that almost all of the relatively recent analyses of the brains of EL victims failed to find any molecular evidence that influenza caused the neurological lesions (see: Reid AH, McCall SJM, and Taubenberger JK. Experimenting on the Past: The Enigma of von Economo’s Encephalitis Lethargica. Journal of Neuropathology & Experimental Neurology, 2001; Vol. 60:7. pp. 663-70).

This evidence together does indeed present a strong case against the influenza argument. And, it is important to further highlight that it is extremely difficult scientifically to prove a negative, in this case, to prove that influenza did not cause EL. Nevertheless, there are readily available and reasonable responses to each of the arguments against the influenza hypothesis.

For example, the fact that only a fraction of EL patients clearly remembered having influenza does not mean that all of the others did not have mild forms that they interpreted simply as a “cold.” Similarly, EL may not appear contagious because by the time its symptoms became apparent, the influenza virus was past its contagious phase.

Pertaining to the molecular evidence, there are many possible explanations. Viruses may cause neurological damage via an autoimmune action in which the virus stimulates the body’s own immune system to cause neurological damage. If the influenza virus acted in this manner, there should be no expectation of finding virus particles in the brains of EL victims. Similarly, only a few brains have been studied, often long after death, and thus long-term survival of viruses in the brains of these patients may be very unlikely. That is, the virus may have directly caused the neurological damage and then been eliminated by the body’s immune system before death.

In support of an influenza etiology of EL is that recent evidence (see Johnson’s book) suggests the influenza pandemic began before the earliest reported cases of EL (earlier data had suggested otherwise), and that there is a very strong relationship between children with EL and influenza. The data on children and EL is not extensive, but almost all the studies report that many of the children first had influenza that transitioned into EL.

Certainly the case for an influenza cause of EL is not conclusive. But the case against it is weaker than commonly perceived. Therefore, should there be another avian-based influenza epidemic, it is not out of the question that there would also be a major recurrence of EL.

Professor Joel A. Vilensky, Ph.D.
Department of Anatomy and Cell Biology
Indiana University School of Medicine
Fort Wayne, Indiana 46805


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