Towards a new method for kinematic quantification of bradykinesia in patients with parkinson's disease using triaxial accelerometry

We propose a new kinematic analysis procedure using triaxial accelerometers mounted to the wrist in the assessment of bradykinesia in patients with Parkinson's disease (PD). The deviation of the magnitude of the accelerometer vector signal from the magnitude of the gravitational acceleration is taken as a measure for effective magnitude of the acceleration at the position of the triaxial accelerometer. For low acceleration, two of the three angles describing the orientation of the lower arm can be derived from the accelerometer signal

SPES/SCOPA and MDS-UPDRS: Formulas for converting scores of two motor scales in Parkinson’s disease

AbstractBackgroundMotor impairment in Parkinson’s disease (PD) can be evaluated with the Short Parkinson’s Evaluation Scale/Scales for Outcomes in Parkinson’s disease (SPES/SCOPA) and the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS). The aim of this study was to determine equation models for the conversion of scores from one scale to the other.Methods148 PD patients were evaluated with the SPES/SCOPA-motor and the MDS-UPDRS motor examination. Linear regression was used to develop equation models.ResultsScores on both scales were highly correlated (r = 0.88). Linear regression revealed the following equation models (explained variance: 78%):1.MDS-UPDRS motor examination score = 11.8 + 2.4 ∗ SPES/SCOPA-motor score2.SPES/SCOPA-motor score = −0.5 + 0.3 ∗ MDS-UPDRS motor examination score.ConclusionWith the equation models identified in this study, scores from SPES/SCOPA-motor can be converted to scores from MDS-UPDRS motor examination and vice versa

Does Deep Brain Stimulation of the Subthalamic Nucleus Prolong Survival in Parkinson's Disease?

Neurological Motor Disorder

Loss of integrity and atrophy in cingulate structural covariance networks in Parkinson's disease

Neuro Imaging Researc

Altered Whole-Brain and Network-Based Functional Connectivity in Parkinson's Disease

Neuro Imaging Researc

Optical Hand Tracking: A Novel Technique for the Assessment of Bradykinesia in Parkinson's Disease

Neurological Motor Disorder

Transcriptomic signatures associated with regional cortical thickness changes in Parkinson's disease

Cortical atrophy is a common manifestation in Parkinson's disease (PD), particularly in advanced stages of the disease. To elucidate the molecular underpinnings of cortical thickness changes in PD, we performed an integrated analysis of brain-wide healthy transcriptomic data from the Allen Human Brain Atlas and patterns of cortical thickness based on T1-weighted anatomical MRI data of 149 PD patients and 369 controls. For this purpose, we used partial least squares regression to identify gene expression patterns correlated with cortical thickness changes. In addition, we identified gene expression patterns underlying the relationship between cortical thickness and clinical domains of PD. Our results show that genes whose expression in the healthy brain is associated with cortical thickness changes in PD are enriched in biological pathways related to sumoylation, regulation of mitotic cell cycle, mitochondrial translation, DNA damage responses, and ER-Golgi traffic. The associated pathways were highly related to each other and all belong to cellular maintenance mechanisms. The expression of genes within most pathways was negatively correlated with cortical thickness changes, showing higher expression in regions associated with decreased cortical thickness (atrophy). On the other hand, sumoylation pathways were positively correlated with cortical thickness changes, showing higher expression in regions with increased cortical thickness (hypertrophy). Our findings suggest that alterations in the balanced interplay of these mechanisms play a role in changes of cortical thickness in PD and possibly influence motor and cognitive functions.Neuro Imaging Researc