Structural white matter alterations as compensatory mechanisms in Parkinson's disease: A systematic review of diffusion tensor imaging studies

Abstract

Compensation is described as normal or near to normal performance in Parkinson's disease (PD), despite the ongoing neural loss. Functional compensation typically proceeds in an inverse U-shaped manner: compensation initiates in the prodromal phase, followed by an increasing episode until plateauing and diminishes in the advanced stages of the disease. The first evidence of the structural compensation was reported by functional magnetic resonance imaging studies. Recent studies, which have used diffusion tensor imaging (DTI) as the basis for their investigation, have shown improved white matter diffusional properties both in motor-and non-motorrelated structures in association with improved clinical scores in patients with PD.The majority of DTI studies have demonstrated microstructural compensation in the prodromal/early stages of PD at the regional scale. However, there have been reports of compensation in later stages of the disease and the whole-brain/network scale that are probably due to the heterogeneous nature of PD. Although serving as a promising beginning to characterize compensation, lots remain to be clarified in understanding the underlying mechanisms of compensation and its structural pattern in PD. The existing knowledge gap necessitates studies that their main research questions are focused on structural compensation. This requirement becomes more apparent because structural compensation evidence has mostly emerged from the post hoc analysis of data and incidental findings of studies. Thus, future studies are required to investigate compensatory microstructural changes in PD to clarify the exact underlying mechanisms. These studies would also provide a basis to develop clinical improvements in the early diagnosis and management of PD. K E Y W O R D S compensation, diffusion tensor imaging, FA, MD, Parkinson's disease, white matter | 1399 SANJARI MOGHADDAM et Al.

An Integrative Nomogram for Identifying Early-Stage Parkinson's Disease Using Non-motor Symptoms and White Matter-Based Radiomics Biomarkers From Whole-Brain MRI

“…Directionality refers to a specific route or angle of the nerve fasciculus. In normal WM, nerve fibers are properly oriented and regulated; nevertheless, when myelin is damaged, the neural structure may be disrupted (Yu et al, 2004), consistent with the white matter damage observed even in patients with early-stage PD in previous studies using advanced MRI technologies, such as DTI (Bergamino et al, 2020;Sanjari Moghaddam et al, 2020), showing that structural changes in the WM may underlie the clinical and pathologic heterogeneity of PD and cause relative cognitive impairment. Therefore, WM is a promising brain tissue to provide new insights that will be important for the early diagnosis of PD.…”

Convolutional Neural Network Optimize the Application of Diffusion Kurtosis Imaging in Parkinson’s Disease

“…For the TBSS analysis, increased FA values were observed in the brain white matter such as anterior thalamic radiation, inferior longitudinal fasciculus, superior longitudinal fasciculus, corticospinal tract, and inferior fronto-occipital fasciculus with both methods and agreed with previous studies 13,[39][40][41] . It has been shown that increased FA in these white matters correlated with better olfactory function and lower motor severity 42 . Thus, these increased diffusional properties of white matter might be a re ection of microstructural compensation 42 .…”

“…It has been shown that increased FA in these white matters correlated with better olfactory function and lower motor severity 42 . Thus, these increased diffusional properties of white matter might be a re ection of microstructural compensation 42 .…”

Brain White-Matter Degeneration Due to Aging and Parkinson Disease as Revealed by Double Diffusion Encoding

“…The absence of these interaction effects in the present study may be attributed to the relatively small sample size which was not optimally matched regarding male/female ratio. Fourth, the majority of patients had relatively long disease duration and were already under medication, and therefore we could not quantify the effects of medication ( Atkinson-Clement et al, 2017 ) and/or the non-linear (U-shaped) trajectories presumably related to neuronal compensation ( Sanjari Moghaddam et al, 2020 ). Lastly, the scan–rescan repeatability should ideally be measured in a cohort similar to the patients because motion artifacts might be severer in these subjects than in young and healthy subjects.…”