scholarly journals Postencephalitic Parkinsonism

2020 ◽  
Author(s):  
Keyword(s):  
Postencephalitic Parkinsonism

scholarly journals No Metagenomic Evidence of Causative Viral Pathogens in Postencephalitic Parkinsonism Following Encephalitis Lethargica

2021 ◽  
Vol 9 (8) ◽  
pp. 1716
Author(s):  
Dániel Cadar ◽  
Kurt A. Jellinger ◽  
Peter Riederer ◽  
Sabrina Strobel ◽  
Camelia-Maria Monoranu ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Neuronal Loss ◽  
Unknown Etiology ◽  
Next Generation ◽  
Encephalitis Lethargica ◽  
Tissue Samples ◽  
Viral Pathogen ◽  
Postencephalitic Parkinsonism ◽  
Generation Sequencing ◽  
Post Infectious

Postencephalitic parkinsonism (PEP) is a disease of unknown etiology and pathophysiology following encephalitis lethargica (EL), an acute-onset polioencephalitis of cryptic cause in the 1920s. PEP is a tauopathy with multisystem neuronal loss and gliosis, clinically characterized by bradykinesia, rigidity, rest tremor, and oculogyric crises. Though a viral cause of EL is likely, past polymerase chain reaction-based investigations in the etiology of both PEP and EL were negative. PEP might be caused directly by an unknown viral pathogen or the consequence of a post-infectious immunopathology. The development of metagenomic next-generation sequencing in conjunction with bioinformatic techniques has generated a broad-range tool for the detection of unknown pathogens in the recent past. Retrospective identification and characterization of pathogens responsible for past infectious diseases can be successfully performed with formalin-fixed paraffin-embedded (FFPE) tissue samples. In this study, we analyzed 24 FFPE brain samples from six patients with PEP by unbiased metagenomic next-generation sequencing. Our results show that no evidence for the presence of a specific or putative (novel) viral pathogen was found, suggesting a likely post-infectious immune-mediated etiology of PEP.

scholarly journals Tauopathies: A Distinct Class of Neurodegenerative Diseases

2007 ◽  
Vol 10 (2) ◽  
pp. 3-14 ◽  
Author(s):  
M Ozansoy ◽  
A Başak
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurofibrillary Tangles ◽  
Neuronal Loss ◽  
Corticobasal Degeneration ◽  
Chromosome 17 ◽  
Cell Degeneration ◽  
Distinct Class ◽  
Postencephalitic Parkinsonism ◽  
Tau Isoforms ◽  
Niemann Pick

Tauopathies: A Distinct Class of Neurodegenerative DiseasesNeurodegenerative diseases are characterized by neuronal loss and intraneuronal accumulation of fibrillary materials, of which, neurofibrillary tangles (NFT) are the most common. Neurofibrillary tangles also occur in normal aging and contain the hyperphosphorylated microtubule-associated protein tau. A detailed presentation is made of the molecular bases of Alzheimer's disease (AD), postencephalitic parkinsonism, amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) of Guam, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), Pick's disease, frontotemporal dementia (FTD), Down's syndrome, myotonic dystrophy (DM) and Niemann-Pick Type C (NPC) disease, which are considered to be common tauopathies. The unique human tau gene extends over 100 kb of the long arm of chromosome 17 and contains 16 exons. The human brain contains six tau isoforms that contain from 352 to 441 amino acids. To date, 34 pathogenic tau mutations have been described among 101 families affected by FTD with parkinsonism linked to chromosome 17 (FTDP-17). These mutations may involve alternative splicing of exon 10 that lead to changes in the proportion of 4-repeat- and 3-repeat-tau isoforms, or may modify tau interactions with microtubules. Tau aggregates differ in degree of phosphorylation and in content of tau isoforms. Five classes of tauopathies have been defined depending on the type of tau aggregates. The key event in tauopathies is the disorganization of the cytoskeleton, which is based on mutations/polymorphisms in the tau gene and lead to nerve cell degeneration. In this review, tauopathies as a distinct class of neurodegenerative diseases are discussed with emphasis on their molecular pathology and genetics.

A neuropathologic study of long-term, Economo-type postencephalitic parkinsonism with a prolonged clinical course

1996 ◽  
Vol 50 (2) ◽  
pp. 79-84
Author(s):  
KATSUYOSHI MIZUKAMI ◽  
MEGUMI SASAKI ◽  
HIROYASU SHIRAISHI ◽  
KENJI IKEDA ◽  
KENJI KOSAKA
Keyword(s):  
Clinical Course ◽  
Postencephalitic Parkinsonism

An autopsy case of postencephalitic parkinsonism of von Economo type: Some new observations concerning neurofibrillary tangles and astrocytic tangles

2000 ◽  
Vol 20 (2) ◽  
pp. 143-148 ◽  
Author(s):  
Takashi Haraguchi ◽  
Hideki Ishizu ◽  
Seishi Terada ◽  
Yasushi Takehisa ◽  
Yasuyuki Tanabe ◽  
...  
Keyword(s):  
Neurofibrillary Tangles ◽  
Autopsy Case ◽  
Postencephalitic Parkinsonism

scholarly journals Anatomy and Pathology of the Basal Ganglia

1987 ◽  
Vol 14 (S3) ◽  
pp. 363-372 ◽  
Author(s):  
P.L. McGeer ◽  
E.G. McGeer ◽  
S. Itagaki ◽  
K. Mizukawa
Keyword(s):  
Amino Acids ◽  
Basal Ganglia ◽  
Neuronal Degeneration ◽  
Signs And Symptoms ◽  
Substantia Nigra Pars Compacta ◽  
Huntington's Chorea ◽  
Reactive Microglia ◽  
Hla Dr ◽  
Infectious Origin ◽  
Postencephalitic Parkinsonism

ABSTRACT:Neurotransmitters of the basal ganglia are of three types: I, amino acids; II, amines; and III, peptides. The amino acids generally act ionotropically while the amines and peptides generally act metabotropically. There are many examples of neurotransmitter coexistence in basal ganglia neurons. Diseases of the basal ganglia are characterized by selective neuronal degeneration. Lesions of the caudate, putamen, subthalamus and substantia nigra pars compacta occur, respectively, in chorea, dystonia, hemiballismus and parkinsonism. The differing signs and symptoms of these diseases constitute strong evidence of the functions of these various nuclei. Basal ganglia diseases can be of genetic origin, as in Huntington's chorea and Wilson's disease, of infectious origin as in Sydenham's chorea and postencephalitic parkinsonism, or of toxic origin as in MPTP poisoning. Regardless of the etiology, the pathogenesis is often regionally concentrated for reasons that are poorly understood. From studies on Parkinson and Huntington disease brains, evidence is presented that a common feature may be the expression of HLA-DR antigen on reactive microglia in the region where pathological neuronal dropout is occurring.

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