Electroencephalography and Clinical Neurophysiology/Evoked Potentials Section
Main articleSomatosensory evoked potentials at rest and during movement in Parkinson's disease: evidence for a specific apomorphine effect on the frontal N30 wave☆
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Cited by (64)
Clinical neurophysiology of Parkinson's disease and parkinsonism
2022, Clinical Neurophysiology PracticeCitation Excerpt :However, some studies did not confirm this finding (Garcia et al., 1995; Drory et al., 1998). Several studies showed that dopaminergic treatments such as apomorphine or levodopa (Rossini et al., 1993; Cheron et al., 1994; Ulivelli et al., 1999) and bilateral STN or GPi DBS (Pierantozzi et al., 1999) increased the N30 SEP amplitude. Consequentially, the frontal N30 SEP has been suggested as a dopamine-dependent physiological marker of basal ganglia modulation of non-primary motor cortical generators of this SEP (Cheron, 1999).
Low- and high-frequency subcortical SEP amplitude reduction during pure passive movement
2015, Clinical NeurophysiologyCitation Excerpt :Moreover, in the curarized patient the SEP traces are free of muscle artefact, thus very reliable responses can be obtained by averaging a low number of trials. The study of PD patients is not expected to be relevant for the physiological meaning of the present results, since a previous study showed that the effect of movement on SEP amplitude is similar in both PD patients and healthy subjects (Rushton et al., 1981; Cheron et al., 1994). In conclusion, our study suggests that movement per se can reduce the SEP amplitude.
Sensorimotor and cognitive involvement of the beta-gamma oscillation in the frontal N30 component of somatosensory evoked potentials
2015, NeuropsychologiaCitation Excerpt :The amplitude of the N30 component is specifically decreased in patients with Parkinson's disease (Rossini et al., 1993; Cheron et al., 1994) and increased in patients with dystonia (Reilly et al., 1992; Kanovský et al., 1997). The injection of apomorphine, or electrical stimulation of the globus pallidus or the subthalamic nucleus, momentarily induces a selective increase of N30 amplitude and a reduction of clinical signs in patients with Parkinson's disease (Cheron et al., 1994; Rossini et al., 1995; Pierantozzi et al., 1999; Onofrj et al., 1995). In clinical practice, the N30 frontal component is therefore considered to be a reliable physiological index for modulatory loop control (dopaminergic dependent) exerted by the basal ganglia on the cortical mantle (Cheron, 1999; Murase et al., 2000; Arahata et al., 2007; Fukuda et al., 2003; Beniczky et al., 2007).
Somatosensory input to non-primary motor areas is enhanced during preparation of cued contraterlateral finger sequence movements
2015, Behavioural Brain ResearchFrontal phasic and oscillatory generators of the N30 somatosensory evoked potential
2011, NeuroImageCitation Excerpt :Conversely, N30 amplitude has been found to be increased in dystonia (Kanovsky et al., 1997; Reilly et al., 1992). Moreover, there has been much discussion on the application of this SEP wave as a physiological index for modulatory loop control (dopaminergic dependent) exerted by the basal ganglia on the cortical mantle based on the reported effect of dopaminergic and deep brain stimulation treatments on N30 amplitude in Parkinsonian patients (Cheron, 1999; Cheron et al., 1994; Onofrj et al., 1995; Pierantozzi et al., 1999). Recent clinical data seem to corroborate this type of modulation (Arahata et al., 2007; Beniczky et al., 2007; Fukuda et al., 2003; Murase et al., 2000).
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This study was supported by the Fonds National de la Recherche Scientifique (FNRS) of Belgium and by a grant from the Philippe and Thérèse Lefêbre S Fund.
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We thank Mrs. Christiane Busson for secretarial assistance, Mrs. Marie-Pierre Dufief, Mr. Michel Baligniez and Mr. Bernard Foucart for technical assistance, and Mrs. Sally Petrequin for revising the English text.