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We tested the hypothesis that Gilles de la Tourette syndrome (GTS) is characterized by perturbed connectivity within cortico-subcortical motor networks. To this end, we performed a dynamic causal modelling (DCM) analysis of fMRI data collected during a finger opposition task in 24 normal controls and 24 GTS patients. The DCM analysis allowed us to assess whether any GTS-specific patterns of brain activity were related to intrinsic and/or to task-dependent connectivity. While no abnormalities were found for task-dependent connectivity, intrinsic connectivity was abnormally increased in the premotor network, with stronger connections from the supplementary motor area (SMA), from the dorsolateral premotor cortex and from the putamen to the right superior frontal gyrus, an area where GTS showed over-activation in a previous univariate analysis. We also found a positive correlation between the connectivity strength from the right basal ganglia to the right primary motor cortex (M1) and disease severity measured by the Yale Global Tic Severity Scale (YGTSS). This pattern was mirrored by a negative correlation between the connection strength from the right SMA to the right area M1 and the YGTSS score. These two reverse correlation effects showed a specific relationship with individual disease severity: the greater the imbalance between subcortical and premotor connectivity towards area M1, the higher the YGTSS score. These results reveal the existence of perturbed intrinsic connectivity patterns in the motor networks of GTS patients with two competing forces operating in a tug of war-like mechanism: aberrant subcortical afferents to M1, compensated for by inputs from the premotor cortex.

In the past years, local field potential (LFP) signals recorded from the subthalamic nucleus (STN) in patients undergoing deep brain stimulation (DBS) for Parkinson's disease (PD) disclosed that DBS has a controversial effect on STN beta oscillations recorded 2-7 days after surgery for macroelectrode implantation. Nothing is known about these DBS-induced oscillatory changes 30 days after surgery. We recorded STN LFPs during ongoing DBS in 7 patients with PD, immediately (hyperacute phase) and 30 days (chronic phase) after surgery. STN LFP recordings showed stationary intranuclear STN beta LFP activity in hyperacute and chronic phases, confirming that beta peaks were also present in chronic recordings. Power spectra of nuclei with significant beta activity (54% of the sample) showed that it decreased significantly during DBS (p=0.021) under both recording conditions. The time course of beta activity showed more evident DBS-induced changes in the chronic than in the hyperacute phase (p=0.014). DBS-induced changes in STN beta LFPs in patients undergoing DBS in chronic phase provide useful information for developing a new neurosignal-controlled adaptive DBS system.

Pathological gambling (PG) is an impulse control disorder that manifests in 2.2–7% of patients with Parkinson's disease (PD). Although the underlying neural mechanisms remain controversial, parkinsonian patients with PG show enhanced risk propensity, especially when assuming dopamine agonist drugs. The dopaminergic reward circuit, a neural network that participates in developing and monitoring motivated behaviours,1 includes the subthalamic nucleus (STN). Local field potentials (LFPs) recorded from macroelectrodes implanted in the STN for deep brain stimulation (DBS) show specific low-frequency oscillations in patients with PD with impulsive control disorders at rest and in patients with PG during the preparation of conflictual economics decisions.2 ,3 No study has yet investigated STN involvement in monetary reward processing, namely the phase that follows economics decisions, when participants face the outcome of their choice in patients with PD. Besides helping to understand the mechanisms underlying PG, this knowledge could promote the optimisation of therapies for impulse control disorders. We investigated the STN's role in risk-related monetary reward in parkinsonian patients. To do so, we studied the reward-related STN LFPs changes in patients with PD with and without PG engaged in an economics decision task. We enrolled 12 patients with PD 4 days after STN DBS macroelectrode positioning surgery as described elsewhere3 (for clinical details, see table 1 from Ref. 3, patients number 1–4, 8–12, 14, 15, 17). Of the 12 patients, 6 met the criteria for PG according to the Diagnostic and Statistical Manual of Mental Disorders (DSM IV-TR). All patients gave informed consent. The study was conducted in accordance with the Declaration of Helsinki and was approved by the institutional review board. Patients were tested with the economics decision task (figure 1A,C) during bilateral STN LFP recording from DBS macroelectrode contact pair 0–2. Figure 1 (A) The economics decision task. Each trial comprised …

Although ample evidence suggests that high-frequency deep brain stimulation (DBS) is an effective therapy in patients with Tourette syndrome (TS), its pathophysiology and the neurophysiological mechanisms underlying these benefits remain unclear. The DBS targets mainly used to date in TS are located within the basal ganglia-thalamo-cortical circuit compromised in this syndrome: the medial and ventral thalamic nuclei, which are way stations within the circuit, the globus pallidus and the nucleus accumbens. Neuronal activity can be electrophysiologically recorded from deep brain structures during DBS surgery (intraoperative microrecordings) or within few days after DBS electrode implantation (local field potentials, LFPs). Recordings from the thalamus in patients with TS showed that the power in low-frequency oscillations (2-15 Hz) was higher than power in high frequency oscillations (

New adaptive systems for deep brain stimulation (DBS) could in the near future optimize stimulation settings online so as to achieve better control over the clinical fluctuations in Parkinson's disease (PD). Local field potentials (LFPs) recorded from the subthalamic nucleus (STN) in PD patients show that levodopa and DBS modulate STN oscillations. Because previous research has shown that levodopa and DBS variably influence beta LFP activity (8-20 Hz), we designed this study to find out how they affect low-frequency (LF) oscillations (2-7 Hz). STN LFPs were recorded in 19 patients with PD during DBS, after levodopa medication, and during DBS and levodopa intake combined. We investigated the relationship between LF modulations, DBS duration and levodopa intake. We also studied whether LF power depended on disease severity, the patient's clinical condition and whether LF modulations were related to electrode impedances. LF power increased during DBS, after levodopa intake and under both experimental conditions combined. The LF power increase correlated with the levodopa-induced clinical improvement and the higher the electrode impedance, the greater was the LF power change. These data suggest that the LF band could be useful as a control neurosignal for developing novel adaptive DBS systems for patients with PD.