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This review compared electrophysiological data obtained in nonhuman primate models of TS and Parkinson's disease \cite{26180116}. This paper focuses on identifying possible mechanisms to account for the reason why high-frequency GPi-DBS is effective for treating both a hyper- and a hypokinetic disorder. This article focuses on the possibility that excessive synchrony and pathological low-frequency oscillations (LFO) impairs activation in the motor regions that receive input from the basal ganglia. There is also some evidence 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 the phasic inhibitons in the GPi for TS patients. It is hypothesized that in both medical conditions aberrant output is minimized whiler the population-averaged firing rate is maintained.   | **Title** | **Comment** |  |:----------|:------------|  | \citep{25342253} | Deep TMS add-on for intractable TS |  |  Challenges for DBS study designs\cite{25882028} | The various obstacles to creating randomized, blinded studies with appropriate controls for a variety of factors are described briefly.  ### Other treatment