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\citet{26180116} reviewed electrophysiological data obtained in nonhuman primate models of TS and in Parkinson disease, with the hope of identifying possible mechanisms to account for the efficacy of high-frequency GPi-DBS in both a hyper- and a hypokinetic movement disorder. This article focuses on the possibility that excessive synchrony and pathological low-frequency oscillations (LFO) impair activation in the motor regions that receive input from the basal ganglia. There is also some evidence that synchronous oscillatory activity and excess LFO contribute to TS. DBS effectiveness is considered to occur because population-scale firing rates are maintained allowing proper encoding of desired movement. When used with Parkinson patients, DBS suppresses excess LFO in the GPE in addition to the GPI. GPI-DBS is theorized to suppress the phasic activations in the GPe and phasic inhibitions in the GPi for TS patients. It is hypothesized that in both medical conditions aberrant output is minimized while the population-averaged firing rate is maintained.   \citet*{26110808} have provided a general review of DBS for movement disorders and also describe some of the recent technological advances (i.e., electrode design; rechargable implantable pulse generators; closed-loop,adaptive,stimulation).  \citet{25882028} discuss various obstacles to carrying out randomized, blinded studies of DBS with appropriate controls. \citet{25925326} summarize research describing neural abnormalities associated with TS and the effects of DBS. They also discuss how the findings relate to models of cortico-basal ganglia function.  ### Other treatment