Atypical parkinsonism, parkinsonism-plus syndromes and secondary parkinsonian disorders

Author(s):  
Joseph Jankovic ◽  
Mark Hallett ◽  
Michael S. Okun ◽  
Cynthia Comella ◽  
Stanley Fahn ◽  
...  
2005 ◽  
Vol 32 (06) ◽  
Author(s):  
K Winge ◽  
H Stimpel ◽  
KK Nielsen ◽  
L Friberg ◽  
L Werdelin

2021 ◽  
Author(s):  
Gerard Saranza ◽  
Emilio Q. Villanueva ◽  
Anthony E. Lang

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 656
Author(s):  
Dariusz Koziorowski ◽  
Monika Figura ◽  
Łukasz M. Milanowski ◽  
Stanisław Szlufik ◽  
Piotr Alster ◽  
...  

Parkinson's disease (PD), dementia with Lewy body (DLB), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD) and multiple system atrophy (MSA) belong to a group of neurodegenerative diseases called parkinsonian syndromes. They share several clinical, neuropathological and genetic features. Neurodegenerative diseases are characterized by the progressive dysfunction of specific populations of neurons, determining clinical presentation. Neuronal loss is associated with extra- and intracellular accumulation of misfolded proteins. The parkinsonian diseases affect distinct areas of the brain. PD and MSA belong to a group of synucleinopathies that are characterized by the presence of fibrillary aggregates of α-synuclein protein in the cytoplasm of selected populations of neurons and glial cells. PSP is a tauopathy associated with the pathological aggregation of the microtubule associated tau protein. Although PD is common in the world's aging population and has been extensively studied, the exact mechanisms of the neurodegeneration are still not fully understood. Growing evidence indicates that parkinsonian disorders to some extent share a genetic background, with two key components identified so far: the microtubule associated tau protein gene (MAPT) and the α-synuclein gene (SNCA). The main pathways of parkinsonian neurodegeneration described in the literature are the protein and mitochondrial pathways. The factors that lead to neurodegeneration are primarily environmental toxins, inflammatory factors, oxidative stress and traumatic brain injury.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Minyoung Oh ◽  
Narae Lee ◽  
Chanwoo Kim ◽  
Hye Joo Son ◽  
Changhwan Sung ◽  
...  

AbstractDelayed phase 18F-FP-CIT PET (dCIT) can assess the striatal dopamine transporter binding to detect degenerative parkinsonism (DP). Early phase 18F-FP-CIT (eCIT) can assess the regional brain activity for differential diagnosis among parkinsonism similar with 18F-FDG PET. We evaluated the diagnostic performance of dual phase 18F-FP-CIT PET (dual CIT) and 18F-FDG PET compared with clinical diagnosis in 141 subjects [36 with idiopathic Parkinson’s disease (IPD), 77 with multiple system atrophy (MSA), 18 with progressive supranuclear palsy (PSP), and 10 with non-DP)]. Visual assessment of eCIT, dCIT, dual CIT, 18F-FDG and 18F-FDG PET with dCIT was in agreement with the clinical diagnosis in 61.7%, 69.5%, 95.7%, 81.6%, and 97.2% of cases, respectively. ECIT showed about 90% concordance with non-DP and MSA, and 8.3% and 27.8% with IPD and PSP, respectively. DCIT showed ≥ 88% concordance with non-DP, IPD, and PSP, and 49.4% concordance with MSA. Dual CIT showed ≥ 90% concordance in all groups. 18F-FDG PET showed ≥ 90% concordance with non-DP, MSA, and PSP, but only 33.3% concordance with IPD. The combination of 18F-FDG and dCIT yielded ≥ 90% concordance in all groups. Dual CIT may represent a powerful alternative to the combination of 18F-FDG PET and dCIT for differential diagnosis of parkinsonian disorders.


2004 ◽  
Vol 10 ◽  
pp. S19-S26 ◽  
Author(s):  
Eduardo Tolosa ◽  
Daniela Calandrella ◽  
Marisol Gallardo

The Lancet ◽  
1999 ◽  
Vol 354 (9188) ◽  
pp. 1472-1473 ◽  
Author(s):  
Irene Litvan

2008 ◽  
Vol 23 (5) ◽  
pp. 727-733 ◽  
Author(s):  
Thomas Eckert ◽  
Chengke Tang ◽  
Yilong Ma ◽  
Nathaniel Brown ◽  
Tanya Lin ◽  
...  

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