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Gait difficulty and postural instability represent motor symptoms in Parkinson disease (PD) that are notoriously difficult to treat. Based on the premise that the pedunculopontine nucleus (PPN) is actively involved in locomotor activity in animals, experimental activation of the PPN has been tried with some success, in locomotion-related outcome measures. However, because stimulation effects have only been modest, it is important to learn more about the physiologic function of the PPN in humans.
Deep brain stimulation (DBS) has become an established and efficient treatment option for advanced PD and other movement disorders. Moreover, DBS provides a unique opportunity to study functional properties of subcortical brain nuclei by taking advantage of the ability of awake patients to perform certain motor tasks. In particular, local field potentials (LFPs) can be recorded directly from the DBS electrodes in the few days that follow implantation, since the DBS-electrode leads are externalized prior to connection to the subcutaneous stimulator. LFPs reflect the summed dendritic synaptic activity of a large number of neurons within a limited volume of neuronal tissue “seen” by the recording electrode.
In this issue of Neurology®, Tsang and coworkers1 use this approach to study the function of the PPN in a cohort of patients with PD examined on and off l-DOPA. In the understandable absence of recordings from healthy people, the parkinsonian ON-state was taken as a surrogate for a normal state of the motor system. Comparison between the medication ON- and OFF-states was used to …
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