Abstract
Idiopathic rapid eye movement sleep behavior disorder (iRBD) is a condition that often evolves into Parkinson's disease (PD). Therefore, by monitoring iRBD it is possible to track the neurodegeneration of individuals who may progress to PD. Here we aimed at piloting the characterization of brain tissue properties in mid-brain subcortical regions of 10 healthy subjects, 8 iRBD, and 9 early-diagnosed PD. We used a battery of magnetic resonance imaging (MRI) contrasts at 3 T, including adiabatic and non-adiabatic rotating frame techniques developed by our group, along with diffusion tensor imaging (DTI) and resting-state fMRI. Adiabatic T1ρ and T2ρ, and non-adiabatic RAFF4 (Relaxation Along a Fictitious Field in the rotating frame of rank 4) were found to have lower coefficient of variations and higher sensitivity to detect group differences as compared to DTI parameters such as fractional anisotropy and mean diffusivity. Significantly longer T1ρ were observed in the amygdala of PD subjects vs. controls, along with a trend of lower functional connectivity as measured by regional homogeneity, thereby supporting the notion that amygdalar dysfunction occurs in PD. Significant abnormalities in reward networks occurred in iRBD subjects, who manifested lower network strength of the accumbens. In agreement with previous studies, significantly longer T1ρ occurred in the substantia nigra compacta of PD vs. controls, indicative of neuronal degeneration, while regional homogeneity was lower in the substantia nigra reticulata. Finally, other trend-level findings were observed, i.e., lower RAFF4 and T2ρ in the midbrain of iRBD subjects vs. controls, possibly indicating changes in non-motor features as opposed to motor function in the iRBD group. We conclude that rotating frame relaxation methods along with functional connectivity measures are valuable to characterize iRBD and PD subjects, and with proper validation in larger cohorts may provide pathological signatures of iRBD and PD.
Highlights
Idiopathic rapid eye movement (REM) sleep behavior disorder is a sleep disorder associated with abnormal pontomedullary synuclein protein. Idiopathic rapid eye movement sleep behavior disorder (iRBD) evolves into Parkinson’s disease (PD) or another synucleinopathy, e.g., dementia with Lewy bodies (LBD) or multiple system atrophy (MSA), in up to 90% of cases (Schenck et al, 1986, 1996; Boeve et al, 2001; Luk et al, 2012; Boeve, 2013; Bunzeck et al, 2013)
Clinical assessments were performed on anti-parkinsonian medications and included the National Institute of Neurological Disorders and Stroke (NINDS) Common Data Element PD medical and family history, demographic information, the Hamilton Anxiety and Depression Rating Scales (Hamilton, 1959, 1960, 1980), United States version of the Parkinson disease questionnaire (PDQ-39) that reflects upon quality of life (Bushnell and Martin, 1999), the Unified Parkinson Disease Rating Scale (UPDRS), the Schwab and England, and Hoehn and Yahr (Fahn and Elton, 1987; Goetz et al, 2007, 2008; Dibble et al, 2010)
We piloted for the first time the multi-slice mapping of rotating frame adiabatic T1ρ and T2ρ and non-adiabatic RAFF4 on a 3 Tesla scanner for human brain studies, which here involved control subjects along with non-demented iRBD and PD subjects
Summary
Idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD) is a sleep disorder associated with abnormal pontomedullary synuclein protein. iRBD evolves into Parkinson’s disease (PD) or another synucleinopathy, e.g., dementia with Lewy bodies (LBD) or multiple system atrophy (MSA), in up to 90% of cases (Schenck et al, 1986, 1996; Boeve et al, 2001; Luk et al, 2012; Boeve, 2013; Bunzeck et al, 2013). It is thought that the α-synuclein pathology in more caudal brainstem regions in iRBD ascends to the substantia nigra (SN) of the midbrain as the disease evolves into PD or other synuclein disorders (Boeve, 2013). Previous studies have focused on evaluating structural approaches such as diffusion tensor imaging (DTI) and voxelbased morphometry (VBM) in patients with PD. This has included work that showed changes in DTI fractional anisotropy (FA) (Menke et al, 2009, 2010; Vaillancourt et al, 2009; Peran et al, 2010; Du et al, 2011) and mean diffusivity (MD) (Kamagata et al, 2012) in the substantia nigra of patients with PD. Our group previously employed novel microstructural imaging methods to map the SN (Michaeli et al, 2007; Nestrasil et al, 2010), as well as other brainstem and subcortical regions, in PD (Karagulle Kendi et al, 2008; Tuite et al, 2012)
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