Paradoxical kinesia may no longer be a paradox waiting for 100 years to be unraveled.

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder mainly characterized by bradykinesia and akinesia. Interestingly, these motor disabilities can depend on the patient emotional state. Disabled PD patients remain able to produce normal motor responses in the context of urgent or externally driven situations or even when exposed to appetitive cues such asmusic. To describe this phenomenon Souques coined theterm "paradoxical kinesia" a century ago. Since then, the mechanisms underlying paradoxical kinesia are still unknown due to a paucity of valid animal models that replicate this phenomenon. To overcome this limitation, we established two animal models of paradoxical kinesia. Using these models, we investigated the neural mechanisms of paradoxical kinesia, with the results pointing tothe inferior colliculus (IC) as a key structure. Intracollicular electrical deep brain stimulation, glutamatergic and GABAergic mechanisms may be involved in the elaboration of paradoxical kinesia. Since paradoxical kinesia might work by activation of some alternative pathway bypassing basal ganglia, we suggest the IC as a candidate to be part of this pathway.