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Abstract: Fourteen patients, suffering from chronic pain resistant to pharmacological treatment, underwent epidural electrode implant on the cervical spinal cord (CSC) for neuromodulation. After the median nerve stimulation, somatosensory evoked potentials (SEPs) were recorded from the epidural electrode contacts, from the frontal and the parietal regions contralateral to the stimulated side, from an electrode placed over the sixth cervical vertebra and from the Erb''s point. SEPs were recorded at rest and during a voluntary flexion–extension movement of the stimulated wrist. The epidural electrode contacts recorded a triphasic potential (P1–N1–P2). The epidural potential amplitude was significantly decreased during voluntary movement compared with the rest, thus suggesting that the effect of movement on SEPs occurs also at CSC level. [Copyright &y& Elsevier]

Objectives To investigate the effect of pure passive movement on both cortical and subcortical somatosensory evoked potentials (SEPs). Methods Median nerve SEPs were recorded in 8 patients suffering from Parkinson’s disease (PD) and two patients with essential tremor. PD patients underwent electrode implantation in the subthalamic (STN) nucleus (3 patients) and pedunculopontine (PPTg) nucleus (5 patients), while 2 patients with essential tremor were implanted in the ventral intermediate nucleus (VIM) of the thalamus. In anesthetized patients, SEPs were recorded at rest and during a passive movement of the thumb of the stimulated wrist from the intracranial electrode contacts and from the scalp. Also the high-frequency oscillations (HFOs) were analyzed. Results Amplitudes of both deep and scalp components were decreased during passive movement, but the reduction was higher at cortical than subcortical level. Also the HFOs were reduced by movement. Conclusion The different amount of the movement-related decrease suggests that the cortical SEP gating is not only the result of a subcortical somatosensory volley attenuation, but a further mechanism acting at cortical level should be considered. Significance Our results are important for understanding the physiological mechanism of the sensory–motor interaction during passive movement. [ABSTRACT FROM AUTHOR]

Objective To investigate the generators of the somatosensory evoked potential (SEP) components recorded from the Pedunculopontine Tegmental nucleus (PPTg). Methods Twenty-two patients, suffering from Parkinson’s disease (PD), underwent electrode implantation in the PPTg area for deep brain stimulation (DBS). SEPs were recorded from the DBS electrode contacts to median nerve stimulation. Results SEPs recorded from the PPTg electrode contacts could be classified in 3 types, according to their waveforms. (1) The biphasic potential showed a positive peak (P16) whose latency (16.05 ± 0.61 ms) shifted of 0.18 ± 0.07 ms from the lower to the upper contact of the electrode. (2) The triphasic potential showed an initial positive peak (P15) whose latency (15.4 ± 0.2 ms) did not change across the DBS electrode contacts. (3) In the last SEP configuration (mixed biphasic and triphasic waveform), the positive peak was bifid including both the P15 and P16 potentials. Conclusion While the P16 potential is probably generated by the somatosensory volley travelling along the medial lemniscus, the P15 response represents a far-field potential probably generated at the cuneate nucleus level. Significance Our results show the physiological meaning of the somatosensory responses recorded from the PPTg nucleus area. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To investigate the effect of the voluntary movement on the amplitude of the somatosensory evoked potentials (SEPs) recorded by an epidural electrode at level of the dorsal column nuclei (DCN). Methods: Five patients, suffering from chronic pain resistant to pharmacological treatment, underwent an epidural electrode implant at high cervical spinal cord level (C2) for neuromodulation. After tibial nerve stimulation, SEPs were recorded from the epidural electrode contacts, from a Cz lead, and from two electrodes placed over the 12th dorsal vertebra and 4th lumbar vertebra, respectively. SEPs were recorded at rest and during a voluntary flexo-extension movement of the stimulated foot. Beyond the low-frequency SEPs, also the high-frequency oscillations (HFOs), obtained by filtering the recorded traces by means of a 1000–2000Hz bandpass offline, were analysed. Results: The epidural electrode contacts recorded a triphasic potential (P1–N1–P2), whose negative peak showed a latency similar to that of the P30 far-field response obtained from the scalp. The epidural potential amplitude was significantly decreased by the voluntary movement, as compared to the rest (p <0.01). A main HFO peak, identifiable at around 1200Hz, was significantly lower in amplitude during movement than at rest (p =0.008). Conclusions: Our findings suggest that the epidural C2 triphasic wave is a potential arising from DCN. The low-frequency epidural SEP component is subtended by a 1200Hz HFO, probably generated by post-synaptic events. Significance: The amplitude reduction of the DCN response during movement is possibly due to decreased excitability of the DCN neurons receiving the somatosensory ascending input. [Copyright &y& Elsevier]

Abstract: Objective: To investigate the effect of the voluntary movement on the amplitude of the somatosensory evoked potentials (SEPs) recorded by an epidural electrode at level of the cervical spinal cord (CSC). Methods: Fourteen patients underwent an epidural electrode implant at CSC level for pain relief. After the median nerve stimulation, SEPs were recorded from the epidural electrode and from 4 surface electrodes (in frontal and parietal regions contralateral to the stimulated side, over the 6th cervical vertebra, and on the Erb’s point). SEPs were recorded at rest and during a voluntary flexo-extension movement of the stimulated wrist. Beyond the low-frequency SEPs, also the high-frequency oscillations (HFOs) were analysed. Results: The epidural electrode contacts recorded a triphasic potential (P1–N1–P2), whose negative peak showed the same latency as the cervical N13 response. The epidural potential amplitude was significantly decreased during the voluntary movement, as compared to the rest. Two main HFOs were identifiable: (1) the 1200Hz HFO which was significantly lower in amplitude during movement than at rest, and (2) the 500Hz HFO which was not modified by the voluntary movement. Conclusions: The low-frequency cervical SEP component is subtended by HFOs probably generated by: (1) postsynaptic potentials in the dorsal horn neurones (1200Hz), and (2) presynaptic ascending somatosensory inputs (500Hz). Significance: Our findings show that the voluntary movement may affect the somatosensory input processing also at CSC level. [Copyright &y& Elsevier]

Objective: To investigate whether the reduction of amplitude of the scalp somatosensory evoked potentials (SEPs) during movement (gating) is due to an attenuation of the afferent volley at subcortical level.Methods: Median nerve SEPs were recorded from 9 patients suffering from Parkinson''s disease, who underwent implant of intracerebral (IC) electrodes in the subthalamic nucleus or in the globus pallidum. SEPs were recorded from Erb''s point ipsilateral to stimulation, from the scalp surface and from the IC leads, at rest and during a voluntary flexo-extension movement of the stimulated wrist. The recorded IC traces were submitted to an off-line filtering by a 300–1500 bandpass to obtain the high-frequency SEP bursts.Results: IC leads recorded a triphasic component (P1–N1–P2) from 14 to 22 ms of latency. The amplitudes of the scalp N20, P20 and N30 potentials and of the IC triphasic component were significantly decreased during movement, while the peripheral N9 amplitude remained unchanged. Also the IC bursts, whose frequency was around 1000 Hz, were reduced in amplitude by the voluntary movement.Conclusions: Since the IC triphasic component is probably generated by neurons of the thalamic ventro-postero-lateral nucleus, which receive the somatosensory afferent volley, the P1–N1 amplitude reduction during movement suggests that the gating phenomenon involves also the subcortical structures. [Copyright &y& Elsevier]