Abstract
Analysis of the amplitude of low frequency BOLD signal fluctuations (ALFF) in the resting state has recently been used to study the dynamics of intrinsic neural activity. Several studies have also suggested its potential as a biomarker for neuropsychiatric disease. In the current study, we quantified ALFF to determine changes in intrinsic neural oscillations in patients with Parkinson's disease (PD) on and off L-DOPA. Twenty-four PD patients and 24 healthy age-matched controls participated in the study. PD patients underwent two resting state fMRI sessions, either ON a controlled dose of L-DOPA or following a placebo pill (OFF). Control participants underwent one test session. We found that there was increased amplitude of low frequency BOLD signal oscillations for PD patients OFF L-DOPA in the primary and secondary motor areas, and in the middle and medial prefrontal cortices. L-DOPA significantly reduced the amplitude of low frequency oscillations within these regions. The degree of ALFF in the premotor cortex predicted patients' motor performance as measured by the Grooved Pegboard task, such that greater ALFF was associated with poorer performance. These results are in line with the pathophysiology of PD, which shows changes in neural oscillations. Thus, frequency domain analyses of resting state BOLD fMRI signals may provide a useful means to study the pathophysiology of PD and the physiology of the brain's dopaminergic pathways.
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with loss of dopaminergic neurons in the substantia nigra pars compacta and the ventral tegmental area with degeneration of the striatal nerve terminals (Bernheimer et al., 1973; Kish et al, 1988; Frey et al, 1996; Rakshi et al, 1999; Braak et al, 2006)
We hypothesized that L-DOPA would reduce the abnormality of signal oscillations in PD patients
We found that there was an abnormal elevation of amplitude of low frequency BOLD signal fluctuations (ALFF) power in PD within the primary and secondary motor regions and the prefrontal cortex (PFC)
Summary
Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with loss of dopaminergic neurons in the substantia nigra pars compacta and the ventral tegmental area with degeneration of the striatal nerve terminals (Bernheimer et al., 1973; Kish et al, 1988; Frey et al, 1996; Rakshi et al, 1999; Braak et al, 2006). Several studies show changes in low frequency neural oscillations (0.3–2.5 Hz) in rodent models of PD (Magill et al, 2001; Tseng et al, 2001; Belluscio et al, 2003; Walters et al., 2007) These studies have shown elevation of synchronous activation between cortical and basal ganglia neurons (Tseng et al., 2001) or an augmentation of oscillatory activity within basal ganglia nuclei (Magill et al, 2001; Belluscio et al, 2003; Walters et al., 2007) at low frequencies. Frontiers in Systems Neuroscience patients showed a widespread slowing of oscillatory brain activity reflected as an increase in the power of neural activity at the low frequency ranges such as the theta and low alpha bands (Soikkeli et al, 1991; Bosboom et al, 2006; Stoffers et al, 2007; Moran et al., 2008). Other studies show prominent increases in beta band oscillations (Kuhn et al, 2004, 2006; Foffani et al, 2005) which are suppressed by dopaminergic treatments (Brown et al, 2001; Levy et al, 2002)
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