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James M. Henry - One of the best experts on this subject based on the ideXlab platform.
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Influenza RNA not Detected in Archival Brain Tissues from Acute Encephalitis Lethargica Cases or in Postencephalitic Parkinson Cases (2001;60:696–704)
Journal of Neuropathology & Experimental Neurology, 2001Co-Authors: James M. HenryAbstract:Influenza RNA not Detected in Archival Brain Tissues from Acute Encephalitis Lethargica Cases or in postencephalitic parkinsonism Cases We are in complete agreement with professor K. Jellinger's observations and conclusions. The protean clinical manifestations of acute Encephalitis Lethargica (EL) presented a polymorphic differential quandary at the time of its initial description, prompting von Economo to consolidate the disease entity into …
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experimenting on the past the enigma of von economo s Encephalitis Lethargica
Journal of Neuropathology and Experimental Neurology, 2001Co-Authors: Ann H Reid, Sherman Mccall, James M. Henry, Jeffery K TaubenbergerAbstract:Encephalitis Lethargica (EL) was a complex and mysterious disease that appeared around the same time as the great influenza pandemic of 1918. The contemporaneous relationship of the 2 diseases led to speculation that they were causally related. Contemporary and subsequent observers conjectured that the influenza virus, directly responsible for the deaths of more than 20 million people, might also have been the cause of EL. A review of the extensive literature by observers of the EL epidemic suggests that most contemporary clinicians, epidemiologists, and pathologists rejected the theory that the 1918 influenza virus was directly responsible for EL. Disappearance of the acute form of EL during the 1920s has precluded direct study of this entity. However, modern molecular biology techniques have made it possible to examine archival tissue samples from victims of the 1918 pandemic in order to detect and study the genetic structure of the killer virus. Similarly, tissue samples from EL victims can now be examined for evidence of infection by the 1918 influenza virus.
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influenza rna not detected in archival brain tissues from acute Encephalitis Lethargica cases or in postencephalitic parkinson cases
Journal of Neuropathology and Experimental Neurology, 2001Co-Authors: Sherman Mccall, James M. Henry, Ann H Reid, Jeffery K TaubenbergerAbstract:Encephalitis Lethargica (EL) was a mysterious epidemic. temporally associated with the 1918 Spanish influenza pandemic. Numerous symptoms characterized this disease, including headache, diplopia, fever, fatal coma, delirium, oculogyric crisis, lethargy, catatonia, and psychiatric symptoms. Many patients who initially recovered subsequently developed profound, chronic parkinsonism. The etiologic association of influenza with EL is controversial. Five acute EL autopsies and more than 70 postencephalitic parkinsonian autopsies were available in the Armed Forces Institute of Pathology (AFIP) tissue repository. Two of these 5 acute EL cases had histopathologic changes consistent with that diagnosis. The remaining 3 cases were classified as possible acute EL cases as the autopsy material was insufficient for detailed histopathologic examination. RNA lysates were prepared from 29 CNS autopsy tissue blocks from the 5 acute cases and 9 lysates from blocks containing substantia nigra from 2 postencephalitic cases. RNA recovery was assessed by amplification of beta-2-microglobulin mRNA and 65% of the tissue blocks contained amplifiable RNA. Reverse transcription-polymerase chain reaction (RT-PCR) for influenza matrix and nucleoprotein genes was negative in all cases. Thus, it is unlikely that the 1918 influenza virus was neurotropic and directly responsible for the outbreak of EL.
Joel Vilensky - One of the best experts on this subject based on the ideXlab platform.
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Encephalitis Lethargica von economo s Encephalitis
Handbook of Clinical Neurology, 2014Co-Authors: Joseph R. Berger, Joel VilenskyAbstract:Abstract In the midst of the Great War (World War I), a peculiar neurologic disease swept large parts of the world in an epidemic fashion. The illness, Encephalitis Lethargica or von Economo's Encephalitis, was characterized by both an acute and chronic phase. The former typically arose on the heels of febrile upper respiratory infection and was characterized by somnolence, asthenia, ocular palsies, and a wide variety of movement disorders. The chronic phase was a common, although not invariable, sequela and occurred months to years later. It was most often characterized by parkinsonism, referred to as postencephalitic parkinsonism, and through the middle of the 20th century may have been responsible for as many as one-half of all parkinsonism cases. This disorder differed from idiopathic Parkinson's disease by the presence of oculogyric crises, alterations in sleep cycle, respiratory disturbances, corticospinal tract findings, and its appearance in young persons. Pathologic studies of Encephalitis Lethargica revealed a polioEncephalitis with predominant involvement of the diencephalon and mesencephalon. The precise etiology of this disorder remains a conundrum. Most investigators suspect a viral etiology. An association with the almost concurrently occurring pandemic influenza epidemic has been proposed, but the preponderance of evidence does not fully support that etiology. Sporadic cases of postencephalitic parkinsonism continue to be reported. There is nothing in the history of medicine to compare with the phantasmagoria of disorder manifested in the course of this strange malady … Into the maze of contradictory phenomena it seemed almost impossible to read anything like a rationalized order of events which might be termed a disease entity (McKenzie, 1927).
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Encephalitis Lethargica during and after the epidemic
2010Co-Authors: Joel VilenskyAbstract:TITLE PAGE COPYRIGHT PAGE TABLE OF CONTENTS CONTRIBUTORS PROLOGUE (STEELE) FOREWORD (SACKS) PREFACE (VILENSKY) 1. Introduction (Vilensky/Gilman) 2. Encephalitis Lethargica During the Epidemic Period (Vilensky/Gilman) 3. Epidemiology (Marlowe/Owens/Vilensky/Cook) 4. Pre-1917 History of Encephalitis Lethargica (Foley/Stevens) 5. Post Epidemic Period Encephalitis Letharigca (Vilensky/Duvoisin/Mukhamedzyanov) 6. Transmissibility (Contagiousness) of Encephalitis Lethargica (Vilensky/Owen) 7. Chronic Encephalitis Lethargica: Postencephalitic Parkinsonism (Vilensky/Gilman) 8. Oliver Sacks, Awakenings and Postencephalitic Parkinsonism (VilenskyDuvoisin/Gilman) 9. Etiology of Encephalitis Lethargica (Vilensky/McCall) 10. Neuropathology of Acute and Chronic Encephalitis Lethargica (Vilensky/Anderson/Duvoisin/Josephs/ Mukhamedzyanov) 11. Self-Reports of Acute and Chronic Encephalitis Lethargica (Vilensky/Cameron/Duvoisin) 12. Conclusions (Vilensky/Gilman)
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A historical analysis of the relationship between Encephalitis Lethargica and postencephalitic parkinsonism: A complex rather than a direct relationship
Movement disorders : official journal of the Movement Disorder Society, 2010Co-Authors: Joel Vilensky, Sid Gilman, Sherman MccallAbstract:Postencephalitic parkinsonism has been considered unique among disorders with parkinsonian features because it is believed to have a unitary etiology associated with the virus that presumably caused Encephalitis Lethargica. Careful analysis of the historical record, however, suggests that this relationship is more complex than commonly perceived. In most cases, the diagnosis of acute Encephalitis Lethargica was made post hoc, and virtually any catarrh-like illness was considered to have represented Encephalitis Lethargica, often after an oral history-taking that was undoubtedly subject to patient recall and physician bias. Also, postencephalitic parkinsonism and oculogyric crises were not recognized as sequelae to Encephalitis Lethargica until well after other sequelae such as movement disorders and mental disturbances had been identified (see previous paper). We suggest here that the relationship between Encephalitis Lethargica and postencephalitic parkinsonism is not simplistic, i.e., Encephalitis Lethargica was not solely responsible for the etiology of postencephalitic parkinsonism, thus aligning the latter with most other parkinsonian disorders that are now believed to have multiple causes.
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Does the historical literature on Encephalitis Lethargica support a simple (direct) relationship with postencephalitic Parkinsonism
Movement disorders : official journal of the Movement Disorder Society, 2010Co-Authors: Joel Vilensky, Sid Gilman, Sherman MccallAbstract: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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Encephalitis Lethargica and Postencephalitic Parkinsonism
Encyclopedia of Movement Disorders, 2010Co-Authors: Joel Vilensky, Roger C. DuvoisinAbstract:Encephalitis Lethargica (EL) was an epidemic disease of the 1920s that had many different forms, but was most typically characterized by sleep disorders (hyersomnolence and/or insomnia). EL was also associated with postencephalitic Parkinsonism, which could develop at any time during the disease process, even many years after apparent recovery. Although various infectious, parainfectious, and toxicologic agents have been postulated to have caused EL, no etiologic agent has been firmly associated with the disorder.
Paul Foley - One of the best experts on this subject based on the ideXlab platform.
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The centennial lesson of Encephalitis Lethargica.
Neurology, 2018Co-Authors: Bart Lutters, Paul Foley, Peter J. KoehlerAbstract:We commemorate the centenary of Constantin von Economo9s description of Encephalitis Lethargica, a mysterious disease that had a significant effect on 20th-century neuroscience. In the acute phase, Encephalitis Lethargica was marked by intractable somnolence, which von Economo attributed to lesions in the diencephalon, thereby paving the way for future efforts to localize the regulation of sleep in the subcortical brain. At the same time, neuropathologic findings in postencephalitic parkinsonism affirmed the role of the substantia nigra in the pathophysiology of parkinsonism. The occurrence of psychiatric symptoms in patients with Encephalitis Lethargica—such as mood disorders, obsessive-compulsive behavior, and bradyphrenia—drew attention to the organic basis of mental illness.
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what caused Encephalitis Lethargica
2018Co-Authors: Paul FoleyAbstract:As you can see, we are still in the field of hypothesis. Perhaps the etiologic problem of Lethargica (as with many other diseases with unknown agents, but which also share the characteristics of infectious diseases) can be clarified only after modifying and broadening current bacteriological methodology, which has, in essence, not markedly advanced since the time of Robert Koch, and that, according to the bold statement of Grumbach, has now proven incompatible with the possibility of further progress in the etiological study of infection. Fernando Rietti, 1935 (p. 26)
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the neuropathology of Encephalitis Lethargica
2018Co-Authors: Paul FoleyAbstract:Precise knowledge of the histological substrate of epidemic Encephalitis, it appears to me, is indispensable not only for understanding the clinical presentation during the acute phase and the entire course of the disease, but also for understanding the severe after-effects. Heinrich Pette, 1942.
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the psychiatry of Encephalitis Lethargica
2018Co-Authors: Paul FoleyAbstract:An entirely new outlook for psychiatry and neurology has been opened, new research possibilities which, it is to be hoped, will bring us closer to understanding psychoses and neuroses. EL is thus not only a new disease in itself, but it has afforded us entirely unexpected, novel insights into the psychologic and physiologic mysteries of the mechanisms of the mind, knowledge that will perhaps also be of significant influence outside the world of medicine. Constantin von Economo, 1923.
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the nature of acute Encephalitis Lethargica
2018Co-Authors: Paul FoleyAbstract:Some epidemic diseases, according to still mysterious laws, after they have wrought damage with an extravagant symptomatology, slumber for years, before again awakening; they confuse those observers who, having forgotten the old descriptions, see them revive, and cannot order them in the frameworks of pathology which they are familiar. Paul Sainton, 1920(a)
Sherman Mccall - One of the best experts on this subject based on the ideXlab platform.
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evidence for an enterovirus as the cause of Encephalitis Lethargica
BMC Infectious Diseases, 2012Co-Authors: Robert R Dourmashkin, Glynis Dunn, Victor Castano, Sherman MccallAbstract:The epidemic of Encephalitis Lethargica (EL), called classical EL, was rampant throughout the world during 1917–1926, affecting half a million persons. The acute phase was lethal for many victims. Post-encephalitic parkinsonism (PEP) affected patients for decades. Our purpose was to investigate the cause of classical EL by studying the few available brain specimens. Cases of PEP and modern EL were also studied. Transmission electron microscopy (TEM) and immunohistochemistry were employed to examine brain from four classical EL cases, two modern EL cases and one PEP case. Standard methods for TEM, immunohistochemistry and RTPCR were applied. 27 nm virus-like particles (VLP) were observed in the cytoplasm and nuclei of midbrain neurons in all classical EL cases studied. Large (50 nm) VLP and 27 nm intranuclear VLP were observed in the modern EL cases and the PEP case. Influenza virus particles were not found. VLP were not observed in the control cases. TEM of cell cultures inoculated with coxsackievirus B4 and poliovirus revealed both small and large intranuclear virus particles and small cytoplasmic particles, similar to the VLP in EL neurons. In the EL brains, nascent VLP were embedded in putative virus factories and on endoplasmic reticulum (ER). The VLP in the cases of classical EL survived, whereas ribosomes underwent autolysis due to the lack of refrigeration and slow formaldehyde fixation of whole brain. The VLP were larger than ribosomes from well preserved brain. Immunohistochemistry of classical EL cases using anti-poliovirus and anti-coxsackievirus B polyclonal antibodies showed significant staining of cytoplasm and nuclei of neurons as well as microglia and neuropil. Purkinje cells were strongly stained. A 97-bp RNA fragment of a unique virus was isolated from brain tissue from acute EL case #91558. Sequence analysis revealed up to 95% identity to multiple human Enteroviruses. Additional cases had Enterovirus positive reactions by real time PCR. The data presented here support the hypothesis that the VLP observed in EL tissue is an Enterovirus.
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A historical analysis of the relationship between Encephalitis Lethargica and postencephalitic parkinsonism: A complex rather than a direct relationship
Movement disorders : official journal of the Movement Disorder Society, 2010Co-Authors: Joel Vilensky, Sid Gilman, Sherman MccallAbstract:Postencephalitic parkinsonism has been considered unique among disorders with parkinsonian features because it is believed to have a unitary etiology associated with the virus that presumably caused Encephalitis Lethargica. Careful analysis of the historical record, however, suggests that this relationship is more complex than commonly perceived. In most cases, the diagnosis of acute Encephalitis Lethargica was made post hoc, and virtually any catarrh-like illness was considered to have represented Encephalitis Lethargica, often after an oral history-taking that was undoubtedly subject to patient recall and physician bias. Also, postencephalitic parkinsonism and oculogyric crises were not recognized as sequelae to Encephalitis Lethargica until well after other sequelae such as movement disorders and mental disturbances had been identified (see previous paper). We suggest here that the relationship between Encephalitis Lethargica and postencephalitic parkinsonism is not simplistic, i.e., Encephalitis Lethargica was not solely responsible for the etiology of postencephalitic parkinsonism, thus aligning the latter with most other parkinsonian disorders that are now believed to have multiple causes.
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Does the historical literature on Encephalitis Lethargica support a simple (direct) relationship with postencephalitic Parkinsonism
Movement disorders : official journal of the Movement Disorder Society, 2010Co-Authors: Joel Vilensky, Sid Gilman, Sherman MccallAbstract: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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experimenting on the past the enigma of von economo s Encephalitis Lethargica
Journal of Neuropathology and Experimental Neurology, 2001Co-Authors: Ann H Reid, Sherman Mccall, James M. Henry, Jeffery K TaubenbergerAbstract:Encephalitis Lethargica (EL) was a complex and mysterious disease that appeared around the same time as the great influenza pandemic of 1918. The contemporaneous relationship of the 2 diseases led to speculation that they were causally related. Contemporary and subsequent observers conjectured that the influenza virus, directly responsible for the deaths of more than 20 million people, might also have been the cause of EL. A review of the extensive literature by observers of the EL epidemic suggests that most contemporary clinicians, epidemiologists, and pathologists rejected the theory that the 1918 influenza virus was directly responsible for EL. Disappearance of the acute form of EL during the 1920s has precluded direct study of this entity. However, modern molecular biology techniques have made it possible to examine archival tissue samples from victims of the 1918 pandemic in order to detect and study the genetic structure of the killer virus. Similarly, tissue samples from EL victims can now be examined for evidence of infection by the 1918 influenza virus.
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influenza rna not detected in archival brain tissues from acute Encephalitis Lethargica cases or in postencephalitic parkinson cases
Journal of Neuropathology and Experimental Neurology, 2001Co-Authors: Sherman Mccall, James M. Henry, Ann H Reid, Jeffery K TaubenbergerAbstract:Encephalitis Lethargica (EL) was a mysterious epidemic. temporally associated with the 1918 Spanish influenza pandemic. Numerous symptoms characterized this disease, including headache, diplopia, fever, fatal coma, delirium, oculogyric crisis, lethargy, catatonia, and psychiatric symptoms. Many patients who initially recovered subsequently developed profound, chronic parkinsonism. The etiologic association of influenza with EL is controversial. Five acute EL autopsies and more than 70 postencephalitic parkinsonian autopsies were available in the Armed Forces Institute of Pathology (AFIP) tissue repository. Two of these 5 acute EL cases had histopathologic changes consistent with that diagnosis. The remaining 3 cases were classified as possible acute EL cases as the autopsy material was insufficient for detailed histopathologic examination. RNA lysates were prepared from 29 CNS autopsy tissue blocks from the 5 acute cases and 9 lysates from blocks containing substantia nigra from 2 postencephalitic cases. RNA recovery was assessed by amplification of beta-2-microglobulin mRNA and 65% of the tissue blocks contained amplifiable RNA. Reverse transcription-polymerase chain reaction (RT-PCR) for influenza matrix and nucleoprotein genes was negative in all cases. Thus, it is unlikely that the 1918 influenza virus was neurotropic and directly responsible for the outbreak of EL.
Angela Vincent - One of the best experts on this subject based on the ideXlab platform.
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n methyl d aspartate receptor antibodies in pediatric dyskinetic Encephalitis Lethargica
Annals of Neurology, 2009Co-Authors: Russell C Dale, Sekhar Pillai, Fabienne Brilot, Richard Webster, Deepak Gill, Sarosh R Irani, Bethan Lang, Angela VincentAbstract:Encephalitis Lethargica (EL) describes an Encephalitis with psychiatric, sleep, and extrapyramidal movement disorders. Dyskinetic and Parkinsonian forms have been described. EL shares clinical features with the anti–N-methyl-D-aspartate receptor (NMDAR-Ab) Encephalitis. We studied 20 sera from pediatric patients with contemporary EL. Ten sera (from 2 males and 8 females, aged 1.3–13 years) and 6/6 cerebrospinal fluid samples were positive for NMDAR-Ab. NMDAR-Ab–positive patients had dyskinesias, agitation, seizures, and insomnia, whereas Parkinsonism and somnolence dominated in the NMDAR-Ab–negative children. We were unable to identify any tumors. The dyskinetic form of EL is an NMDAR-Ab Encephalitis and can affect very young children. Ann Neurol 2009;66:704–709
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n methyl d aspartate receptor antibodies in pediatric dyskinetic Encephalitis Lethargica
Annals of Neurology, 2009Co-Authors: Russell C Dale, Sekhar Pillai, Fabienne Brilot, Richard Webster, Deepak Gill, Sarosh R Irani, Bethan Lang, Angela VincentAbstract:Encephalitis Lethargica (EL) describes an Encephalitis with psychiatric, sleep, and extrapyramidal movement disorders. Dyskinetic and parkinsonian forms have been described. EL shares clinical features with the anti-N-methyl-D-aspartate receptor (NMDAR-Ab) Encephalitis. We studied 20 sera from pediatric patients with contemporary EL. Ten sera (from 2 males and 8 females, aged 1.3-13 years) and 6/6 cerebrospinal fluid samples were positive for NMDAR-Ab. NMDAR-Ab-positive patients had dyskinesias, agitation, seizures, and insomnia, whereas parkinsonism and somnolence dominated in the NMDAR-Ab-negative children. We were unable to identify any tumors. The dyskinetic form of EL is an NMDAR-Ab Encephalitis and can affect very young children.
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Encephalitis Lethargica part of a spectrum of post streptococcal autoimmune diseases
Brain, 2004Co-Authors: Angela VincentAbstract:Encephalitis Lethargica (EL) was first described by von Economo in 1917, shortly after the start of the 1916–1927 epidemic. The patients, mostly children of either sex, characteristically presented with headache and malaise, lethargy, insomnia, and ophthalmoplegia. Some recovered but the others either died during an acute fulminating disorder or developed, insidiously or after a variable period of time, movement and/or psychiatric disorders including Parkinsonism, oculogyric crises, chorea, myoclonus, mutism, catatonia or behavioural problems. Although linked by many observers to the influenza epidemic, the epidemic of EL began earlier and lasted longer, and flu virus has not been found in archival post‐mortem tissue (e.g. McCall et al ., 2001; Lo and Geddes, 2003). Sporadic cases are still reported, but the acute fulminating form seems to have disappeared, and there have been no further reported epidemics. The paper by Dale and colleagues in this issue of Brain describes 20 patients with a condition presenting with sleep disorder, lethargy, Parkinsonism and neuropsychiatric disorders, including mutism, anxiety, depression, obsessions and compulsions (Dale et al ., 2004). The patients ranged between 2 and 69 years of age, but most were children or teenagers. Although we are not told the time between onset and study by the authors, half of the patients had a monophasic illness, and five have made a good recovery, but the others have continuing problems of movement or neuropsychiatric disorders at a follow‐up period of <2 years. The clinical features, the course of the disease, cerebrospinal fluid and imaging studies, and histology in one case, are similar to those in cases …