From among all causes of encephalitis - structural, chemical, and microbiological - it was a difficult task sorting out the many infectious causes of encephalitis by specific causative organism and route of transmission. But with the explosion of scientific knowledge in the late nineteenth and twentieth centuries, many important agents and vectors of encephalitis were identified, among them, the spirochete of syphilis, and the trypanosome of African sleeping sickness, transmitted by sexual contact and tsetse flies, repectively; the bacterial toxin of botulism, from ingested food; the viruses of yellow fever, Japanese B encephalitis, equine encephalitis, transmitted by mosquitoes; the virus of rabies, transmitted by the bite of rabid animals; the viruses of influenza, mumps, and measles, transmitted by the respiratory route; the enteroviruses, transmitted by the fecal-oral route; and, most recently, the human immunodeficiency virus, transmitted by sexual contact and blood.

Adding to the diagnostic confusion generated by these numerous encephalitic microorganisms were the many cases and deaths from stuporous encephalitic reactions to various toxins and drugs, especially Reye's syndrome following the use of aspirin (introduced in 1899) to control the fever and discomfort of influenza, varicella, and other childhood diseases. The role of aspirin in the production of Reye's syndrome has become known only in the last decade.

But the main causative agent of epidemic encephalitis during the pandemic years 1917—26 was the respiratorily spread influenza virus. Successive peaks of encephalitis occurred in European, Asian, African, and American countries from 1918 to about 1926. In the United States, encephalitis lethargica progressed across the country from the east to the west in 1919, just as influenza had the previous year, reaching peak occurrence in New York during January 1919, in Virginia during February, and in Illinois, Louisiana, and Texas during March; whereas in California more cases were reported in April than in any other month, and in Seattle the first encephalitis lethargica cases were reported in October 1919. Although Britain reported its peak number of cases in 1924, this was apparently a reporting artifact - as judged from the mortality pattern during the 1920s.

For too long, medical science has tended to relegate the 1918 influenza-encephalitis lethargica-parkinsonism puzzle to an intellectual ash heap, apparently on the assumption that these epidemics are past history and of little or at least dwindling importance to current and future health. But failure to identify influenza virus as the cause of encephalitis lethargica and parkinsonism has crippled progress toward the understanding of influenza pathology and epidemiology needed to fuel and guide prevention of these elusive but exceedingly important diseases.

According to William Osier, Karl Menninger, and August Wimmer, almost every disease of the central nervous system (CNS) may follow influenza. Thus we should look to the diminutions of CNS structures caused by influenza attacks during earlier life when seeking the keys to prevention of much serious CNS disease, especially senile dementia (Alzheimer's disease).

R. T. Ravenholt

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