Motor-cortical oscillations in early stages of Parkinson's disease

University of Düsseldorf, Medical Faculty, Institute of Clinical Neuroscience and Medical Psychology, Department of Neurology, Düsseldorf, Germany.
The Journal of Physiology (Impact Factor: 5.04). 04/2012; 590(Pt 13):3203-12. DOI: 10.1113/jphysiol.2012.231316
Source: PubMed


Pathophysiological changes in basal ganglia-thalamo-cortical circuits are well established in idiopathic Parkinson's disease (PD). However, it remains open whether such alterations already occur at early stages representing a characteristic neurophysiological marker of PD. Therefore, the present study aims at elucidating changes of synchronised oscillatory activity in early PD patients. In this study, we performed whole-head magnetoencephalography (MEG) in a resting condition and during steady state contraction of the more severely affected forearm in 10 drug–naive, de novo patients, in 10 early-stage patients with chronic medication and in 10 age-matched control subjects. While cortico-muscular coherence (CMC) did not differ between groups, patients showed increased sensori-motor cortical power at beta frequency (13–30 Hz) during rest as well as during isometric contraction compared to controls. In healthy control subjects the power of the contralateral hemisphere was significantly suppressed during isometric contraction. By contrast, both hemispheres were activated equally strongly in de novo patients. In medicated patients, the pattern was found to be reversed. Contralateral beta power was significantly correlated with motor impairment during isometric contraction but not during rest. The present results suggest that the reduced ability of the primary motor cortex to disengage from increased beta band oscillations during the execution of movements is an early marker of PD.

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Available from: Bettina Pollok, Sep 12, 2014
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    • "Of key interest was, furthermore, the response of the sensorimotor beta rhythm, which is a known pathophysiological marker of PD (e.g. Gatev et al., 2006; Hammond et al., 2007; Pollok et al., 2012; Brittain and Brown, 2014), and which is hypothesised to represent an internal likelihood index for pending voluntary action (Engel and Fries, 2010; Jenkinson and Brown, 2011). The magnitude of the movement-related beta amplitude modulation, commonly attenuated in PD (e.g. "
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    ABSTRACT: The basal ganglia play an important role in beat perception and patients with Parkinson’s disease (PD) are impaired in perception of beat-based rhythms. Rhythmic cues are nonetheless beneficial in gait rehabilitation, raising the question how rhythm improves movement in PD.We addressed this question with magneto-encephalography recordings during a choice response task with rhythmic and non-rhythmic modes of stimulus presentation. Analyses focused on (i) entrainment of slow oscillations, (ii) the depth of beta power modulation, and (iii) whether a gain in modulation depth of beta power, due to rhythmicity, is of predictive or reactive nature. The results show weaker phase synchronisation of slow oscillations and a relative shift from predictive to reactive movement-related beta suppression in PD. Nonetheless, rhythmic stimulus presentation increased beta modulation depth to the same extent in patients and controls. Critically, this gain selectively increased the predictive and not reactive movement-related beta power suppression. Operation of a predictive mechanism, induced by rhythmic stimulation, was corroborated by a sensory gating effect in the sensorimotor cortex. The predictive mode of cue utilisation points to facilitation of basal ganglia-premotor interactions, contrasting with the popular view that rhythmic stimulation confers a special advantage in PD, based on recruitment of alternative pathways.
    Full-text · Article · Sep 2015 · Clinical neuroimaging
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    • "activity in the sensorimotor cortex (SMC) is coherent with electromyographic (EMG) activity of the contralateral muscle in the b-band (15–30 Hz) during isometric contraction (Conway et al., 1995; Salenius et al., 1997; Gross et al., 2000; Pohja et al., 2005; Kristeva-Feige et al., 2002; Ushiyama et al., 2010, 2011a,b; Omlor et al., 2007, 2011; Johnson et al., 2011; Perez et al., 2012; Divekar and John, 2013; Mendez-Balbuena et al., 2012; Patino et al., 2008; Pollok et al., 2012). These oscillatory interactions between the cortex and muscle can be assessed by calculation of coherence, which is a measure of linear correlation in the frequency domain. "
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    ABSTRACT: β-Band corticomuscular coherence is suggested as an electrophysiological mechanism that contributes to sensorimotor functioning in the maintenance of steady-state contractions. Converging evidence suggests that not only the descending corticospinal pathway but the ascending sensory feedback pathway is involved in the generation of β-band corticomuscular coherence. The present study aimed to investigate which pathway, descending vs. ascending, contributes more to the stability of muscle contraction, especially for human intrinsic hand muscles.
    Full-text · Article · Oct 2014 · Clinical neurophysiology: official journal of the International Federation of Clinical Neurophysiology
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    • "This may be due to the fact that the majority of studies focus on late-stage patients who are usually taking dopamine replacement therapies which are known to reduce beta power (Silberstein et al., 2005; Kuhn et al., 2006; Ku¨hn et al., 2009; Jenkinson and Brown, 2011) or collapse of cortical beta generation in later stages of the disease. The results presented here confirm those in a previous investigation in early-stage PD patients which did report enhanced beta in M1 contralateral to the most severely affected side (Pollok et al., 2012). Anecdotally, a number of the patients (e.g. "
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    ABSTRACT: In Parkinson's disease (PD), elevated beta (15 - 35 Hz) power in subcortical motor networks is widely believed to promote aspects of PD symptomatology, moreover, a reduction in beta power and coherence accompanies symptomatic improvement following effective treatment with L-DOPA. Previous studies have reported symptomatic improvements that correlate with changes in cortical network activity following GABAA receptor modulation. In this study we have used whole-head magnetoencephalography to characterise neuronal network activity, at rest and during visually cued finger abductions, in unilaterally symptomatic PD and age-matched control participants. Recordings were then repeated following administration of sub-sedative doses of the hypnotic drug zolpidem (0.05 mg/Kg), which binds to the benzodiazepine site of the GABAA receptor. A beamforming based 'virtual electrode' approach was used to reconstruct oscillatory power in primary motor cortex, contralateral and ipsilateral to symptom presentation in PD patients or dominant hand in control participants. In PD patients, contralateral M1 showed significantly greater beta power than ipsilateral M1. Following zolpidem administration contralateral beta power was significantly reduced while ipsilateral beta power was significantly increased resulting in a hemispheric power ratio that approached parity. Furthermore, there was highly significant correlation between hemispheric beta power ratio and UPDRS. The changes in contralateral and ipsilateral beta power were reflected in pre-movement beta desynchronisation and the late post-movement beta rebound. However, the absolute level of movement-related beta desynchronisation was not altered. These results show that low-dose zolpidem not only reduces contralateral beta but also increases ipsilateral beta, whilst rebalancing the dynamic range of M1 network oscillations between the two hemispheres. These changes appear to underlie the symptomatic improvements afforded by low-dose zolpidem.
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