Effects Of Pallidal Deep Brain Stimulation Research Articles

Deep brain stimulation in the globus pallidus modulates pallidal and subthalamic neural oscillations.

Deep brain stimulation (DBS) in the basal ganglia has been introduced to treat movement disorders. The effects of pallidal DBS on the neural oscillations in the globus pallidus interna (GPi) and the subthalamic nucleus (STN) of the same subject remains unclear. In this study, the DBS electrodes were bilaterally implanted in the GPi and STN in patients with Tourette's syndrome (TS). The local field potentials were simultaneously recorded from the GPi and STN during pallidal DBS with 130 Hz, 60 microseconds, and 1V/2V/2.5V voltages. The time-frequency characteristics were analyzed across the conditions of resting, stimulation and post-stimulation. The results showed that alpha and beta oscillation existed in the basal ganglia and the beta oscillation was attenuated by pallidal stimulation. The attenuations are significantly different among 1V/2V/2.5V voltages. The results suggest that beta oscillations may have physiological function in resisting tics in TS. Thus, the oscillation- and symptom-guided intelligent DBS needs to be investigated.

Effect of pallidal deep-brain stimulation on articulation rate in dystonia.

Pallidal deep-brain stimulation of the internal globus pallidus (GPi-DBS) is an effective treatment for dystonia. However, GPi-DBS may cause important stimulation-induced side effects such as hypokinetic dysarthria, which is particularly manifested by articulation rate abnormalities. However, little data regarding the effect of the location of the electrode and stimulation parameters for pallidal stimulation on articulation rate in dystonia is available. Speech data were acquired from 18 dystonic patients with GPi-DBS and 18 matched healthy controls. Each of dystonic patients was tested twice within 1day in both the GPi-DBS ON and GPi-DBS OFF stimulation conditions. Compared to healthy controls, the decreased diadochokinetic rate and slower articulation rate in dystonic patients were observed in both stimulation conditions. No significant differences in speech rate measures between stimulation conditions were detected with no relation to contact localization and stimulation intensity. Our findings do not support the use articulation rate as a surrogate marker of stimulation-induced changes to the speech apparatus in dystonia.

Pallidal Deep-Brain Stimulation Disrupts Pallidal Beta Oscillations and Coherence with Primary Motor Cortex in Parkinson's Disease.

In Parkinson's disease (PD), subthalamic nucleus beta band oscillations are decreased by therapeutic deep-brain stimulation (DBS) and this has been proposed as important to the mechanism of therapy. The globus pallidus is a common alternative target for PD with similar motor benefits as subthalamic DBS, but effects of pallidal stimulation in PD are not well studied, and effects of pallidal DBS on cortical function in PD are unknown. Here, in 20 PD and 14 isolated dystonia human patients of both genders undergoing pallidal DBS lead implantation, we recorded local field potentials from the globus pallidus and in a subset of these, recorded simultaneous sensorimotor cortex ECoG potentials. PD patients had elevated resting pallidal low beta band (13-20 Hz) power compared with dystonia patients, whereas dystonia patients had elevated resting pallidal theta band (4-8 Hz) power compared with PD. We show that this results in disease-specific patterns of interaction between the pallidum and motor cortex: PD patients demonstrated relatively elevated phase coherence with the motor cortex in the beta band and this was reduced by therapeutic pallidal DBS. Dystonia patients had greater theta band phase coherence. Our results support the hypothesis that specific motor phenomenology observed in movement disorders are associated with elevated network oscillations in specific frequency bands, and that DBS in movement disorders acts in general by disrupting elevated synchronization between basal ganglia output and motor cortex.SIGNIFICANCE STATEMENT Perturbations in synchronized oscillatory activity in brain networks are increasingly recognized as important features in movement disorders. The globus pallidus is a commonly used target for deep-brain stimulation (DBS) in Parkinson's disease (PD), however, the effects of pallidal DBS on basal ganglia and cortical oscillations are unknown. Using invasive intraoperative recordings in patients with PD and isolated dystonia, we found disease-specific patterns of elevated oscillatory synchronization within the pallidum and in coherence between pallidum and motor cortex. Therapeutic pallidal DBS in PD suppresses these elevated synchronizations, reducing the influence of diseased basal ganglia on cortical physiology. We propose a general mechanism for DBS therapy in movement disorders: functional disconnection of basal ganglia output and motor cortex by coherence suppression.

Surgical treatment of dystonia

Surgical treatment of dystonia has experienced a tremendous change over the past decade. Whilst selective peripheral denervation is reserved for cervical dystonia refractory to botulinum toxin injections, deep brain stimulation (DBS) of the pallidum has gained a wide scope and presents an elementary column in the treatment of medically refractory patients, nowadays. There is consensus that idiopathic generalized, cervical and segmental dystonia are good indications for DBS, although there is still a paucity of studies providing high-level data according to EBM criteria. Efficacy is maintained on longterm. Several other forms of primary dystonia are still under investigation but it appears that patients with Meige syndrome and myoclonus-dystonia gain also marked benefit. Study of the outcome in secondary dystonia disorders is more complex, in general, but patients with tardive dystonia gain similar improvement than patients with idiopathic dystonia. Overall, the risk profile of pallidal DBS is quite low, and it has been shown to be cognitively safe. The effect of pallidal DBS on non-dystonic extremities has not received much attention, albeit there are hints for a pro-akinetic mechanism. Several questions remain to be solved including optimal programming of stimulation settings, battery drain with high stimulation energies and the elucidation of the mechanisms of DBS in dystonia.