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Somatosensory 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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Abstract

Studies attempting to relate the abnormalities of the frontal N30 components of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We recorded the frontal and parietal SEPs to median nerve stimulation in 2 groups of PD patients: a group of 17 patients presenting the wearing-off phenomenon, and a group of 10 untreated PD patients. The results were compared with a group of 13 healthy volunteers of the same age and with a group of 10 non-parkinsonian patients. All parkinsonian and non-parkinsonian patients were studied before (“off” condition) and after a subcutaneous injection of apomorphine (“on” condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs were also studied for the wearing-off group of PD patients (in states off and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly reduced in the 2 groups of PD patients. We demonstrate that the movement gating ability of the PD patient is preserved in spite of the reduced amplitude of the frontal N30. This result suggests that the specific change in the frontal N30 in PD is not the consequence of a continuous gating of the sensory inflow by a motor corollary discharge. Clinical motor improvement induced by apomorphine was associated with a significant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not statistically modified by the drug. Apomorphine infusion did not change the absolute reduced voltage of the N30 reached during the movement gating. While the frontal N30 component of the non-parkinsonian patients was significantly lower in comparison to healthy subjects, this wave did not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated with the number of off hours per day. This specific apomorphine sensitivity of the frontal N30 was interpreted as a physiological index of the dopaminergic modulatory control exerted on the neuronal structures implicated in the generation of the frontal N30.

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Cited by (64)

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    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

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    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

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    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).

  • Frontal phasic and oscillatory generators of the N30 somatosensory evoked potential

    2011, NeuroImage
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    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.

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