Objective Recent discoveries suggest that it is most likely the coupling of β oscillations (13–30 Hz) and not merely their power that relates to Parkinson disease (PD) pathophysiology. Methods We analyzed power and phase amplitude coupling (PAC) in local field potentials (LFP) recorded from Pallidum after placement of deep brain stimulation (DBS) leads in nineteen PD patients and three patients with dystonia. Results Within GPi, we identified PAC between phase of β and amplitude of high frequency oscillations (200–300 Hz) and distinct β-low γ (40–80 Hz) PAC both modulated by contralateral movement. Resting β-low γ PAC, also present in dystonia patients, inversely correlated with severity of rigidity and bradykinesia (R=−0.44, P=0.028). These findings were specific to the low β band, suggesting a differential role for the two β sub-bands. Conclusions PAC is present across distinct frequency bands within the GPi. Given the presence of low β-low γ PAC in dystonia and the inverse correlation with symptom severity, we propose that this PAC may be a normal pallidal signal. Significance This study provides new evidence on the pathophysiological contribution of local pallidal coupling and suggests similar and distinct patterns of coupling within GPi and STN in PD.

Symptoms in Parkinson’s disease (PD) have been linked to oscillatory activity within the basal ganglia. In humans, such activity has been detected mainly in the local field potentials (LFPs) recorded from electrode contacts used for deep brain stimulation. Although most studies have focused on activity within the subthalamic nucleus (STN), the internal part of the globus pallidus (GPi) is considered an equally efficacious site for therapeutic neuromodulation. Moreover, while most investigations have evaluated changes in oscillatory activity in the beta (12–35 Hz) and gamma (35–100 Hz) bands, our preliminary spectral analysis of LFP signals in the GPi suggested distinct activity at higher frequencies as well. We hypothesized there is a unique LFP signature in the GPi that consists of movement modulated spectral power increases above 100Hz. Using invasive recordings from the GPi of patients undergoing DBS, in addition to confirming increased beta band activity within the GPi of patients with PD, we have identified and characterized a previously undescribed peak between 200–300 Hz centered at approximately 235 Hz, whose height and width but not center frequency are movement modulated. An increase in peak height is not transient, but rather persists for the duration of movement. The 200–300 Hz rhythms in the GPi could have a functional role in the basal ganglia reentrant circuits by encoding output information entering the thalamo-cortical network or by organizing downstream activity for the successful execution of tasks.

Arrays of carbon nanotube (CNT) microelectrodes (nominal geometric surface areas 20-200 μm(2)) were fabricated by photolithography with chemical vapor deposition of randomly oriented CNTs. Raman spectroscopy showed strong peak intensities in both G and D bands (G/D = 0.86), indicative of significant disorder in the graphitic layers of the randomly oriented CNTs. The impedance spectra of gold and CNT microelectrodes were compared using equivalent circuit models. Compared to planar gold surfaces, pristine nanotubes lowered the overall electrode impedance at 1 kHz by 75%, while nanotubes treated in O(2) plasma reduced the impedance by 95%. Cyclic voltammetry in potassium ferricyanide showed potential peak separations of 133 and 198 mV for gold and carbon nanotube electrodes, respectively. The interaction of cultured cardiac myocytes with randomly oriented and vertically aligned CNTs was investigated by the sectioning of myocytes using focused-ion-beam milling. Vertically aligned nanotubes deposited by plasma-enhanced chemical vapor deposition (PECVD) were observed to penetrate the membrane of neonatal-rat ventricular myocytes, while randomly oriented CNTs remained external to the cells. These results demonstrated that CNT electrodes can be leveraged to reduce impedance and enhance biological interfaces for microelectrodes of subcellular size.

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