Suppression of beta oscillations in the subthalamic nucleus following cortical stimulation in humans.

It is unclear how subthalamic nucleus activity is modulated by the cerebral cortex. Here we investigate the effect of transcranial magnetic stimulation (TMS) of the cortex on oscillatory subthalamic local field potential activity in the 8-35 Hz (alpha/beta) band, as exaggerated synchronization in this band is implicated in the pathophysiology of parkinsonism. We studied nine patients with Parkinson's disease (PD) to test whether cortical stimulation can modulate synchronized oscillations in the human subthalamic nucleus. With patients at rest, single-pulse TMS was delivered every 5 s over each primary motor area and supplementary motor area at intensities of 85-115% resting motor threshold. Subthalamic local field potentials were recorded from deep brain stimulation electrodes implanted into this nucleus for the treatment of PD. Motor cortical stimulation suppressed beta activity in the subthalamic nucleus from approximately 0.2 to 0.6 s after TMS (repeated measures anova; main effect of time, P < 0.01; main effect of side, P = 0.03), regardless of intensity. TMS over the supplementary motor area also reduced subthalamic beta activity at 95% (P = 0.05) and 115% resting motor threshold (P = 0.01). The oscillatory activity decreased to 80 +/- 26% of baseline (averaged across sites and stimulation intensities). Suppression with subthreshold stimuli confirmed that these changes were centrally driven and not due to peripheral afference. The results may have implications for mechanisms underlying the reported therapeutic benefits of cortical stimulation.

Detection of signals in modulated and unmodulated noise observed using auditory evoked potentials.

OBJECTIVE: To investigate a neurophysiological correlate of the perceptual enhancement of noise-masked sounds when the masking frequencies have a wide spectral bandwidth and are coherently amplitude-modulated. METHODS: Auditory evoked potentials were recorded to 1 kHz tones (200 ms, 61 dBSPL, SOA 3s) occurring in silence or with 80 dB masking noise, which was either wide-band or narrow-band and either unmodulated or 100% amplitude-modulated by a 17.5 Hz square-wave. In a second study, the tones were timed to coincide alternately with the rise and fall of the masker envelope. RESULTS: N1 and P2 potentials recorded to the unmasked tones were abolished in the presence of the unmodulated masker, but were elicited again with lower amplitude and longer latency when the masker was modulated. No significant effect of the masker bandwidth was observed. Latencies were strongly determined by whether the tones coincided with the rise or fall of the masker envelope, indicating that the responses were only evoked when the instantaneous noise level was low. CONCLUSIONS: The findings demonstrate partial correspondence to the threshold reduction to similar stimuli seen in comodulation masking release (CMR). The dependence of latencies on the phase of the masker envelope is consistent with the 'dip-listening' model of CMR. SIGNIFICANCE: Under these conditions the N1/P2 complex can be viewed as a possible neurophysiological correlate of perceptual CMR.