What caused the 1918–30 Epidemic of Encephalitis Lethargica?

Dourmashkin, R. R.

doi:10.1177/014107689709000916

Cited by 27 publications

(23 citation statements)

References 33 publications

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“…Many of those who recovered from this disease developed post-encephalitic Parkinsonism [9, 25, 31]. The cause of this outbreak of encephalitis has not been positively identified.…”

Section: Introductionmentioning

confidence: 99%

Rotenone and paraquat do not directly activate microglia or induce inflammatory cytokine release

Klintworth

Garden

Xia

2009

Neuroscience Letters

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Both epidemiological and pathological data suggest an inflammatory response including microglia activation and neuro-inflammation in the Parkinsonian brain. Treatments with lipopolysacchride (LPS), rotenone and paraquat have been used as models for Parkinson's disease, as they cause dopaminergic neuron degeneration in culture and in animals. Recent studies have suggested that rotenone and paraquat induce neuro-inflammation, however, it is not known if they can directly activate microglia. Here, we use primary cultured microglia to address this question. Microglia activation was analyzed by morphological changes and release of nitric oxide and inflammatory cytokines. Treatment with LPS was used as a positive control. While LPS induced morphological changes characteristic of microglial activation and release of nitric oxide and inflammatory cytokines, rotenone and paraquat did not. Our results suggest that paraquat and rotenone do not act directly on microglia and that neuro-inflammation and microglial activation in animals treated with these agents is likely non-cell autonomous, and may occur as a result of dopaminergic neuron damage or factors released by neurons and other cells.

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“…Many of those who recovered from this disease developed post-encephalitic Parkinsonism [9, 25, 31]. The cause of this outbreak of encephalitis has not been positively identified.…”

Section: Introductionmentioning

confidence: 99%

Rotenone and paraquat do not directly activate microglia or induce inflammatory cytokine release

Klintworth

Garden

Xia

2009

Neuroscience Letters

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“…The aetiology of EL remains a mystery, although there are several theories concerning possible causes. Such theories include viruses—either a neurotropic virus different from influenza (e.g., polio), or activation of a latent virus, bacteria—poststreptococcal-like illness analogous to chorea and rheumatic fever, toxins, dietary issues due to wartime deprivation, miscellaneous, or “rag bag” diagnosis with the actual incidence being inflated by other conditions, or an autoimmune reaction to a virus [7, 10, 28, 56, 57]. …”

Section: Discussionmentioning

confidence: 99%

The Demise of Poskanzer and Schwab’s Influenza Theory on the Pathogenesis of Parkinson’s Disease

Estupinan

Nathoo

Okun

2013

Parkinson's Disease

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In 1961, David C. Poskanzer and Robert S. Schwab presented a paper, “Studies in the epidemiology of Parkinson's disease predicting its disappearance as a major clinical entity by 1980.” This paper introduced the hypothesis that Parkinson's disease was derived from a single aetiology, the influenza virus. We review the original Poskanzer and Schwab hypothesis that Parkinson's disease was based on the association between the 1918-19 influenza epidemic and the later observation of Parkinsonism in some influenza sufferers. We also further explore the prediction that Parkinson's disease would totally disappear as an entity once original influenza victims were all deceased. Current research has revealed that there are many potential causes and factors important in the occurrence of Parkinson's disease, postencephalitic Parkinsonism, and encephalitis lethargica. Poskanzer and Schwab presented a novel hypothesis; however, it was proven false by a combination of research and time.

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“…Certainly, this variability related to definitional aspects of PEP as well as to the timeframe used to record the patient's history. On the basis of the data in Table 2, it is difficult to accept the premise that the vast majority of EL cases eventually developed PEP as advocated by Duvoisin and Yahr in 1965 46 or the statement by Dourmashkin in 1997 47 that, ''the outstanding motor manifestation [of the chronic form] was the parkinsonian syndrome, present in almost every case.'' Rather, non-PEP sequelae (especially psychiatric) were common during the epidemic period and will likely still be prevalent should EL recur.…”

Section: Historical Review Of El Reports Pertaining To Parkinsonismmentioning

confidence: 99%

“…Rather, non-PEP sequelae (especially psychiatric) were common during the epidemic period and will likely still be prevalent should EL recur. The lack of attention to these non-PEP sequelae 47 have undoubtedly skewed the perception toward accepting a direct relationship between EL and PEP.…”

Section: Historical Review Of El Reports Pertaining To Parkinsonismmentioning

confidence: 99%

Does the historical literature on encephalitis lethargica support a simple (direct) relationship with postencephalitic Parkinsonism?

2010

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This article and the subsequent one suggest that the currently accepted view of a simplistic (direct) relationship between encephalitis lethargica (EL) and postencephalitic Parkinsonism (PEP) is based on a incomplete evaluation of the epidemic period literature. In this article we provide a detailed analysis of the literature from the period that demonstrates that Parkinsonism was not initially part of acute EL symptomatology, that PEP was not typically the prevailing type of chronic EL and that oculogyric crises were never part of acute EL symptomatology and not initially associated with PEP. The second paper uses these finding, and also examines the clinical justifications for concluding that all patients with PEP had prior acute episodes of EL, to reevaluate the presumed direct etiologic relationship between EL and PEP.

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What caused the 1918–30 Epidemic of Encephalitis Lethargica?

Cited by 27 publications

References 33 publications

Rotenone and paraquat do not directly activate microglia or induce inflammatory cytokine release

Rotenone and paraquat do not directly activate microglia or induce inflammatory cytokine release

The Demise of Poskanzer and Schwab’s Influenza Theory on the Pathogenesis of Parkinson’s Disease

Does the historical literature on encephalitis lethargica support a simple (direct) relationship with postencephalitic Parkinsonism?

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