Combined assessment of midbrain hyperechogenicity, hyposmia and motor asymmetry improves diagnostic accuracy in early Parkinson’s disease

2012 ◽  
Vol 12 (8) ◽  
pp. 911-914 ◽  
Author(s):  
Werner Poewe ◽  
Philipp Mahlknecht
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Diagnostic Accuracy ◽  
Motor Asymmetry ◽  
Early Parkinson’S Disease

Diagnostic accuracy of [99mTc]TRODAT-1 SPECT imaging in early Parkinson's disease

2004 ◽  
Vol 10 (6) ◽  
pp. 375-379 ◽  
Author(s):  
K.L Chou ◽  
H.I Hurtig ◽  
M.B Stern ◽  
A Colcher ◽  
B Ravina ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Diagnostic Accuracy ◽  
Spect Imaging ◽  
Early Parkinson’S Disease

scholarly journals The α-Synuclein Origin and Connectome Model (SOC Model) of Parkinson’s Disease: Explaining Motor Asymmetry, Non-Motor Phenotypes, and Cognitive Decline

2021 ◽  
Vol 11 (2) ◽  
pp. 455-474
Author(s):  
Per Borghammer
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cognitive Decline ◽  
Explanatory Power ◽  
Anatomical Location ◽  
Asymmetric Distribution ◽  
Motor Asymmetry ◽  
Parasympathetic Innervation ◽  
Considerable Body ◽  
Dopaminergic Degeneration

A new model of Parkinson’s disease (PD) pathogenesis is proposed, the α-Synuclein Origin site and Connectome (SOC) model, incorporating two aspects of α-synuclein pathobiology that impact the disease course for each patient: the anatomical location of the initial α-synuclein inclusion, and α-synuclein propagation dependent on the ipsilateral connections that dominate connectivity of the human brain. In some patients, initial α-synuclein pathology occurs within the CNS, leading to a brain-first subtype of PD. In others, pathology begins in the peripheral autonomic nervous system, leading to a body-first subtype. In brain-first cases, it is proposed that the first pathology appears unilaterally, often in the amygdala. If α-synuclein propagation depends on connection strength, a unilateral focus of pathology will disseminate more to the ipsilateral hemisphere. Thus, α-synuclein spreads mainly to ipsilateral structures including the substantia nigra. The asymmetric distribution of pathology leads to asymmetric dopaminergic degeneration and motor asymmetry. In body-first cases, the α-synuclein pathology ascends via the vagus to both the left and right dorsal motor nuclei of the vagus owing to the overlapping parasympathetic innervation of the gut. Consequently, the initial α-synuclein pathology inside the CNS is more symmetric, which promotes more symmetric propagation in the brainstem, leading to more symmetric dopaminergic degeneration and less motor asymmetry. At diagnosis, body-first patients already have a larger, more symmetric burden of α-synuclein pathology, which in turn promotes faster disease progression and accelerated cognitive decline. The SOC model is supported by a considerable body of existing evidence and may have improved explanatory power.

scholarly journals Longitudinal Analysis of Multiple Neurotransmitter Metabolites in Cerebrospinal Fluid in Early Parkinson's Disease

2021 ◽  
Author(s):  
Thomas Kremer ◽  
Kirsten I. Taylor ◽  
Juliane Siebourg‐Polster ◽  
Thomas Gerken ◽  
Andreas Staempfli ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrospinal Fluid ◽  
Longitudinal Analysis ◽  
Early Parkinson’S Disease ◽  
Neurotransmitter Metabolites
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