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      Deep learning reveals personalized spatial spectral abnormalities of high delta and low alpha bands in EEG of patients with early Parkinson’s disease

      , , , , , , , , ,
      Journal of Neural Engineering
      IOP Publishing

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          Abstract

          Objective. Parkinson’s disease (PD) is one of the most common neurodegenerative diseases, and early diagnosis is crucial to delay disease progression. The diagnosis of early PD has always been a difficult clinical problem due to the lack of reliable biomarkers. Electroencephalogram (EEG) is the most common clinical detection method, and studies have attempted to discover the EEG spectrum characteristics of early PD, but the reported conclusions are not uniform due to the heterogeneity of early PD patients. There is an urgent need for a more advanced algorithm to extract spectrum characteristics from EEG to satisfy the personalized requirements. Approach. The structured power spectral density with spatial distribution was used as the input of convolutional neural network (CNN). A visualization technique called gradient-weighted class activation mapping was used to extract the optimal frequency bands for identifying early PD. Based on the model visualization, we proposed a novel quantitative index of spectral characteristics, spatial-mapping relative power (SRP), to detect personalized abnormalities in the spatial spectral characteristics of EEG in early PD. Main results. We demonstrated the feasibility of applying CNN to identify the patients with early PD with an accuracy of 99.87% ± 0.03%. The models indicated the characteristic frequency bands (high-delta (3.5–4.5 Hz) and low-alpha (7.5–11 Hz) frequency bands) that are used to identify the early PD. The SRP of these two characteristic bands in early PD patients was significantly higher than that in the control group, and the abnormalities were consistent at the group and individual levels. Significance. This study provides a novel personalized detection algorithm based on deep learning to reveal the optimal frequency bands for identifying early PD and obtain the spatial frequency characteristics of early PD. The findings of this study will provide an effective reference for the auxiliary diagnosis of early PD in clinical practice.

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          An introduction to ROC analysis

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            Movement Disorder Society-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS): scale presentation and clinimetric testing results.

            We present a clinimetric assessment of the Movement Disorder Society (MDS)-sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS-UPDRS). The MDS-UDPRS Task Force revised and expanded the UPDRS using recommendations from a published critique. The MDS-UPDRS has four parts, namely, I: Non-motor Experiences of Daily Living; II: Motor Experiences of Daily Living; III: Motor Examination; IV: Motor Complications. Twenty questions are completed by the patient/caregiver. Item-specific instructions and an appendix of complementary additional scales are provided. Movement disorder specialists and study coordinators administered the UPDRS (55 items) and MDS-UPDRS (65 items) to 877 English speaking (78% non-Latino Caucasian) patients with Parkinson's disease from 39 sites. We compared the two scales using correlative techniques and factor analysis. The MDS-UPDRS showed high internal consistency (Cronbach's alpha = 0.79-0.93 across parts) and correlated with the original UPDRS (rho = 0.96). MDS-UPDRS across-part correlations ranged from 0.22 to 0.66. Reliable factor structures for each part were obtained (comparative fit index > 0.90 for each part), which support the use of sum scores for each part in preference to a total score of all parts. The combined clinimetric results of this study support the validity of the MDS-UPDRS for rating PD.
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              Parkinson disease

              Parkinson disease is the second-most common neurodegenerative disorder that affects 2-3% of the population ≥65 years of age. Neuronal loss in the substantia nigra, which causes striatal dopamine deficiency, and intracellular inclusions containing aggregates of α-synuclein are the neuropathological hallmarks of Parkinson disease. Multiple other cell types throughout the central and peripheral autonomic nervous system are also involved, probably from early disease onwards. Although clinical diagnosis relies on the presence of bradykinesia and other cardinal motor features, Parkinson disease is associated with many non-motor symptoms that add to overall disability. The underlying molecular pathogenesis involves multiple pathways and mechanisms: α-synuclein proteostasis, mitochondrial function, oxidative stress, calcium homeostasis, axonal transport and neuroinflammation. Recent research into diagnostic biomarkers has taken advantage of neuroimaging in which several modalities, including PET, single-photon emission CT (SPECT) and novel MRI techniques, have been shown to aid early and differential diagnosis. Treatment of Parkinson disease is anchored on pharmacological substitution of striatal dopamine, in addition to non-dopaminergic approaches to address both motor and non-motor symptoms and deep brain stimulation for those developing intractable L-DOPA-related motor complications. Experimental therapies have tried to restore striatal dopamine by gene-based and cell-based approaches, and most recently, aggregation and cellular transport of α-synuclein have become therapeutic targets. One of the greatest current challenges is to identify markers for prodromal disease stages, which would allow novel disease-modifying therapies to be started earlier.
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                Author and article information

                Contributors
                Journal
                Journal of Neural Engineering
                J. Neural Eng.
                IOP Publishing
                1741-2560
                1741-2552
                December 24 2021
                December 01 2021
                December 24 2021
                December 01 2021
                : 18
                : 6
                : 066036
                Article
                10.1088/1741-2552/ac40a0
                34875634
                f30a6f3a-0e45-474e-aa59-f02ff5e51d3f
                © 2021

                https://iopscience.iop.org/page/copyright

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