Abstract
Using a fixel-based analysis (FBA), we assessed the fiber-specific white matter (WM) alterations in nonmedicated patients with early-stage Parkinson’s disease (PD) with tremor-dominant (TD; n = 53; mean age, 61.7 ± 8.7 years) and postural instability and gait disorder (PIGD; n = 27; mean age, 57.8 ± 8.1 years) motor subtypes and age- and sex-matched healthy controls (HC; n = 43; mean age, 61.6 ± 9.2 years) from Parkinson’s Progression Markers Initiative dataset. FBA revealed significantly increased macrostructural fiber cross section and a combination of fiber density and cross section metrics within the corticospinal tract in patients with TD-PD compared with HC. Nonetheless, no significant changes in FBA-derived metrics were found in patients with PIGD-PD compared with HC or patients with TD-PD. Our results may provide evidence of WM neural compensation mechanisms in patients with TD-PD marked by increases in fiber bundle size and the ability to relay information between brain regions.
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, mainly characterized by cardinal motor symptoms, including rigidity, resting tremor, and bradykinesia, as manifestations of selective loss of dopaminergic neurons in the substantia nigra pars compacta and the widespread aggregation of αsynuclein in the form of Lewy neurites and Lewy bodies[1]
All subjects were without cognitive decline (Montreal Cognitive Assessment [MoCA] score ≥ 26); the MoCA scores were significantly higher in patients with postural instability and gait disorder (PIGD)-PD than in those with tremor dominant (TD)-PD (P = 0.013), while no significant differences were found between healthy controls (HC) and either patients with TD-PD or PIGD-PD
The mean striatal binding ratio (SBR) of patients with TD-PD and PIGD-PD was significantly lower (P < 0.0001) than in HC, while there was no difference between patients with TD-PD and PIGD-PD
Summary
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, mainly characterized by cardinal motor symptoms, including rigidity, resting tremor, and bradykinesia, as manifestations of selective loss of dopaminergic neurons in the substantia nigra pars compacta and the widespread aggregation of αsynuclein in the form of Lewy neurites and Lewy bodies[1]. Based on predominance of specific motor signs at the time of diagnosis, two main subtypes of Parkinson’s disease (PD) are described: tremor dominant (TD) and postural instability and gait disorder (PIGD)[2]. PIGD-PD is associated with a faster rate of motor decline and weaker response to levodopa treatment[3], while TD-PD is known to have a better prognosis and slower disease progression[2]. Different clinical presentations and progression of the two PD motor subtypes suggest distinct underlying neural mechanisms. While detailed knowledge of the white matter (WM) changes in TD-PD and PIGD-PD, in the early stage, is essential to guide future disease-modifying strategies successfully, to date, the WM structural alterations in TD-PD and PIGD-PD have not been fully elucidated. A recent study in patients with early-stage TD-PD reported greater
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