Postencephalitic Parkinsonism: Unique Pathological and Clinical Features-Preliminary Data

• Published in: Cells (Basel, Switzerland) Switzerland), 2024-09, Vol.13 (18), p.1511
• Main Authors: Strobel, Sabrina, Sian-Hulsmann, Jeswinder, Tappe, Dennis, Jellinger, Kurt, Riederer, Peter, Monoranu, Camelia-Maria
• Format: Article
• Language: English
• Subjects: Age; Aged; Aged, 80 and over; Amyotrophic lateral sclerosis; Autopsy; Basal ganglia; Brain; Brain - pathology; Central nervous system diseases; Chelating agents; cognitive disturbances; Dementia; Development and progression; Disease; Encephalitis; Female; Humans; Immunological memory; Influenza; Iron; Iron - metabolism; iron pathology; Levodopa; Lewy bodies; Li Siguang; Magnetic resonance imaging; Male; Memory; Middle Aged; Movement disorders; Neural networks; Neurodegeneration; Neurodegenerative diseases; Neurofibrillary tangles; Neurons; Neuropathology; Neurophysiology; Neurosciences; Oxidative stress; Parkinson Disease, Postencephalitic - pathology; Parkinson's disease; Parkinsonian Disorders - complications; Parkinsonian Disorders - pathology; Pathology; Patients; postencephalitic parkinsonism; Synuclein; Tau protein; tau Proteins - metabolism; Tremor (Muscular contraction); Viruses
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells13181511

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.