Postencephalitic Parkinsonism: Unique Pathological and Clinical Features—Preliminary Data

Postencephalitic parkinsonism (PEP) is suggested to show a virus-induced pathology, which is different from classical idiopathic Parkinson's disease (PD) as there is no α-synuclein/Lewy body pathology. However, PEP shows a typical clinical representation of motor disturbances. In addition, compared to PD, there is no iron-induced pathology. The aim of this preliminary study was to compare PEP with PD regarding iron-induced pathology, using histochemistry methods on paraffin-embedded post-mortem brain tissue. In the PEP group, iron was not seen, except for one case with sparse perivascular depositions. Rather, PEP offers a pathology related to tau-protein/neurofibrillary tangles, with mild to moderate memory deficits only. It is assumed that this virus-induced pathology is due to immunological dysfunctions causing (neuro)inflammation-induced neuronal network disturbances as events that trigger clinical parkinsonism. The absence of iron deposits implies that PEP cannot be treated with iron chelators. The therapy with L-Dopa is also not an option, as L-Dopa only leads to an initial slight improvement in symptoms in isolated cases.

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Publication Details

Journal
Cells
Published
2024-09-10
DOI
https://doi.org/10.3390/cells13181511
Citations
3
Primary Topic
Parkinson's Disease Mechanisms and Treatments
Type
article
Field-Weighted Citation Impact
1.11
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article

Postencephalitic Parkinsonism: Unique Pathological and Clinical Features—Preliminary Data

Sabrina Strobel, Jeswinder Sian‐Hülsmann, K. A. Jellinger, Peter Riederer et al.
3 citations
Cells
Parkinson's Disease Mechanisms and Treatments
1.11
article

Postencephalitic Parkinsonism: Unique Pathological and Clinical Features—Preliminary Data

Sabrina Strobel, Jeswinder Sian‐Hülsmann, K. A. Jellinger, Peter Riederer, Camelia‐Maria Monoranu, Dennis Tappe
article en
3 citations

Abstract

Postencephalitic parkinsonism (PEP) is suggested to show a virus-induced pathology, which is different from classical idiopathic Parkinson's disease (PD) as there is no α-synuclein/Lewy body pathology. However, PEP shows a typical clinical representation of motor disturbances. In addition, compared to PD, there is no iron-induced pathology. The aim of this preliminary study was to compare PEP with PD regarding iron-induced pathology, using histochemistry methods on paraffin-embedded post-mortem brain tissue. In the PEP group, iron was not seen, except for one case with sparse perivascular depositions. Rather, PEP offers a pathology related to tau-protein/neurofibrillary tangles, with mild to moderate memory deficits only. It is assumed that this virus-induced pathology is due to immunological dysfunctions causing (neuro)inflammation-induced neuronal network disturbances as events that trigger clinical parkinsonism. The absence of iron deposits implies that PEP cannot be treated with iron chelators. The therapy with L-Dopa is also not an option, as L-Dopa only leads to an initial slight improvement in symptoms in isolated cases.

CellsVol. 13(18)
University of Nairobi (KE), University of Southern Denmark (DK), University of Würzburg (DE), Universitätsklinikum Würzburg (DE), Bernhard Nocht Institute for Tropical Medicine (DE)
Openalex Percentile: Top 21%
Parkinson's Disease Mechanisms and Treatments
1.11
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