Longitudinal changes of cortical microstructure in Parkinson's disease assessed with T1 relaxometry

Abstract

BackgroundHistological evidence suggests that pathology in Parkinson's disease (PD) goes beyond nigrostriatal degeneration and also affects the cerebral cortex. Quantitative MRI (qMRI) techniques allow the assessment of changes in brain tissue composition. However, the development and pattern of disease-related cortical changes have not yet been demonstrated in PD with qMRI methods. The aim of this study was to investigate longitudinal cortical microstructural changes in PD with quantitative T1 relaxometry.Methods13 patients with mild to moderate PD and 20 matched healthy subjects underwent high resolution T1 mapping at two time points with an interval of 6.4 years (healthy subjects: 6.5 years). Data from two healthy subjects had to be excluded due to MRI artifacts. Surface-based analysis of cortical T1 values was performed with the FreeSurfer toolbox.ResultsIn PD patients, a widespread decrease of cortical T1 was detected during follow-up which affected large parts of the temporo-parietal and occipital cortices and also frontal areas. In contrast, age-related T1 decrease in the healthy control group was much less pronounced and only found in lateral frontal, parietal and temporal areas. Average cortical T1 values did not differ between the groups at baseline (p = 0.17), but were reduced in patients at follow-up (p = 0.0004). Annualized relative changes of cortical T1 were higher in patients vs. healthy subjects (patients: − 0.72 ± 0.64%/year; healthy subjects: − 0.17 ± 0.41%/year, p = 0.007).ConclusionsIn patients with PD, the development of widespread changes in cortical microstructure was observed as reflected by a reduction of cortical T1. The pattern of T1 decrease in PD patients exceeded the normal T1 decrease as found in physiological aging and showed considerable overlap with the pattern of cortical thinning demonstrated in previous PD studies. Therefore, cortical T1 might be a promising additional imaging marker for future longitudinal PD studies. The biological mechanisms underlying cortical T1 reductions remain to be further elucidated.

Longitudinal quantitative MRI assessment of cortical damage in multiple sclerosis: A pilot study

“…However, accuracy increases when several voxels are combined for analysis, such as in our clusters: Given a total cluster size of 20,139 mm 2 for T 1 and 8016 mm 2 for PD, the expected error levels are much lower than the observed quantitative longitudinal changes. Stability of the method of analysis and of the scanner have been shown in a previous study that assessed longitudinal cortical T 1 changes in Parkinson's disease and healthy control subjects . However, inclusion of a control group would be advantageous for future longitudinal qMRI studies, where independent validation of stability may not be available.…”

“…Stability of the method of analysis and of the scanner have been shown in a previous study that assessed longitudinal cortical T 1 changes in Parkinson's disease and healthy control subjects. 35 However, inclusion of a control group would be advantageous for future longitudinal qMRI studies, where independent validation of stability may not be available.…”

Regional T1 mapping of the whole cervical spinal cord using an optimized MP2RAGE sequence

“…Quantitative mapping of MR longitudinal relaxation time, referred to as T 1 relaxometry, is not only important for the determination of adequate MR sequence parameters, but it also offers tremendous perspectives for structural and pathological tissue characterization in different organs. 1,2 The T 1 relaxation time, or spin-lattice relaxation time, is indeed tissue and field specific, and a growing amount of work supports the use of T 1 mapping as an in vivo marker of tissue microstructure in clinical and neuroscientific research, probing for instance disease-related tissue changes [3][4][5] or developmental plasticity and ageing. [6][7][8] Over the years, numerous MR techniques have been proposed and used to estimate T 1 values.…”

Clinical and Neuropathological Features Associated With Loss of RAB39B

“…We analyzed neuronal oscillatory activity known to be relevant to the pathophysiology of PD. Results: After ultrasound stimulation, mean power intensity in the beta band (13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) Hz) significantly decreased, and the phase-amplitude coupling strength between the beta and high gamma (55-100 Hz) bands and between the beta and ripple (100-200 Hz) bands also became significantly weaker. Parkinson's disease (PD) is a neurodegenerative disease that places a heavy burden on patients and their families 1,2 ; therefore, finding more effective treatments for PD is important.…”