Postencephalitic Parkinson Syndrome after Meningoencephalitis Due to Coxsackie Virus Group B, Type 2

Walters, John

doi:10.1056/nejm196010132631507

Cited by 53 publications

(15 citation statements)

References 18 publications

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“…In addition there have been individual case reports describing the association of different viruses with this disorder. These have included a 54-year-old woman who manifested symptoms of parkinsonism while convalescing from meningoencephalitis due to Coxsackie B virus (Walters, 1960) and similar processes have been described following influenza A (Hudson and Rice, 1990), poliovirus (Bojinov 1971) and measles virus (Alves et al, 1992) infections. The possible involvement of virus infection has also been supported by experimental animal models, Fishman et al (1985) reported a selective attack on the substantia nigra and subthalamic nucleus by a strain of mouse hepatitis virus, and more recently similar features have been described in rats infected with influenza virus (Takahashi et al, 1995).…”

Section: Discussionmentioning

confidence: 98%

A rat model of Parkinson's disease induced by Japanese encephalitis virus

Ogata¹,

Tashiro²,

Nukuzuma³

et al. 1997

J Neurovirol

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In Fischer rats infected with Japanese encephalitis virus (JEV) at 13 days after birth and sacrificed 12 weeks later, the major pathological changes resembled those found in Parkinson's disease. Specifically there was neuronal loss with gliosis which was confined mainly to the zona compacta of the substantia nigra, with a notable absence of lesions in the cerebral cortex and cerebellum. Changes were bilateral being most severe in the central part of the zona compacta. Immunohistochemical studies with anti-tyrosine hydroxylase (TH) demonstrated that the number of TH-positive neurons was significantly decreased in the substantia nigra compared to controls, while comparable numbers of TH-positive neurons were found in the basal ganglia in both JEVtreated rats and age-matched controls. JEV-infected rats showed marked bradykinesia, with significant behavioral improvement being observed following administration of L-DOPA. Immunohistochemical studies failed to detect JEV antigens in any region of the rat brain and the JEV genome was undetectable in the substantia nigra and the cerebral cortex using the reverse transcription-polymerase chain reaction (RT ± PCR). The findings suggest that JEV infection of rats under the conditions described may serve as a model of virus induced Parkinson's Disease.

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Section: Discussionmentioning

confidence: 98%

A rat model of Parkinson's disease induced by Japanese encephalitis virus

Ogata¹,

Tashiro²,

Nukuzuma³

et al. 1997

J Neurovirol

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“…It has also been shown that exposure to the highly pathogenic neurotropic H5N1 influenza virus increases susceptibility to developing PD with an observed onset of post-influenzal encephalopathies (Jang et al, 2009b). Other viruses associated with secondary Parkinsonism include coxsackie virus (Poser et al, 1969;Walters, 1960), Japanese encephalitis B (Ogata et al, 1997), St. Louis virus (Pranzatelli et al, 1994), west Nile virus (Robinson et al, 2003) and human immunodeficiency virus (HIV) (Tse et al, 2004). Infection with Japanese-encephalitis virus (JEV), which occurs predominantly in India, China and Southeast Asia, for a prolonged period is likely to induce PEP (Ogata et al, 2000;Shoji et al, 1993;Tansey et al, 2007).…”

Section: Epidemiological Evidencementioning

confidence: 99%

Contributions of central and systemic inflammation to the pathophysiology of Parkinson's disease

Collins¹,

Toulouse²,

Connor³

et al. 2012

Neuropharmacology

256

153

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“…Acute parkinsonism has been noted after infection with Coxsackie virus [99, 100] although its association with traditional aged-onset idiopathic Parkinson's disease has never been established. As with influenza virus, it is possible that early infection with Coxsackie virus can induce a long lived activation with glial cells that would predispose to oxidative insult much later in life [101].…”

Section: Influenza Virusmentioning

confidence: 99%

Viral parkinsonism

Jang

Boltz

Webster

et al. 2009

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

273

280

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Parkinson's disease is a debilitating neurological disorder characterized that affects 1-2% of the adult population over 55 years of age. For the vast majority of cases, the etiology of this disorder is unknown, although it is generally accepted that there is a genetic susceptibility to any number of environmental agents. One such agent may be viruses. It has been shown that numerous viruses can enter the nervous system, i.e. they are neurotropic, and induce a number of encephalopathies. One of the secondary consequences of these encephalopathies can be parkinsonism, that is both transient as well as permanent. One of the most highlighted and controversial cases of viral parkinsonism is that which followed the 1918 influenza outbreak and the subsequent induction of von Economo's encephalopathy. In this review, we discuss the neurological sequelae of infection by influenza virus as well as that of other viruses known to induce parkinsonism including Coxsackie, Japanese encephalitis B, St. Louis, West Nile and HIV viruses.

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Postencephalitic Parkinson Syndrome after Meningoencephalitis Due to Coxsackie Virus Group B, Type 2

Cited by 53 publications

References 18 publications

A rat model of Parkinson's disease induced by Japanese encephalitis virus

A rat model of Parkinson's disease induced by Japanese encephalitis virus

Contributions of central and systemic inflammation to the pathophysiology of Parkinson's disease

Viral parkinsonism

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