Our findings, in accordance with other recent cognitive research, support the view of the models' inadequacy to explain cognitive deficits seen in PD and the way they are affected by stimulation (Pillon, 2002), consistent with recent studies suggesting that functional surgery in PD could influence cognitive and affective processes (Malapani et al., submitted). The cognitive and behavioral outcome might depend on the exact location of the stimulation (Lombardi et al., 2000), suggesting that it may be crucial to evaluate changes between off and on stimulation on more specific behavioral and cognitive research tools (Ardouin et al., 1999; Jahanashi et al., 2000; Pillon et al., 2000; Saint-Cyr et al., 2000).
The model predicts that high-frequency stimulation in the STn would mimic the effects of DA replacement therapy overall (Bejjani et al., 1997; Limousin et al., 1995a, 1995b), which is not the case here (the encode deficit is alleviated by levodopa, but not by STn DBS). Moreover, if the STn overactivity is driven by a reduced neural activity in the GPe, as predicted by the model, then DBS in the GPe should produce effects similar to those of STn DBS. In contrast, DBS in the GPi would be expected to alleviate the coupling phenomenon on the decode and maybe the slowed encode, via its concomitant effect in reducing the excitation driven by the indirect pathway, allowing the inhibitory control of the direct one to take place. In sum, our results neither replicated the dopaminomimetic effect of STn DBS nor showed effects that would be easy to reconcile with the two functionally and anatomically segregated pathways, depicted by the classical model of basal ganglia circuitry (Albin et al., 1989; DeLong, 1990). Although these results may suggest that the cognitive and motor basal ganglia circuits are not as anatomically and functionally segregated as previously considered, some functional segregation does exist within the circuitry, since learning remains distorted with STn stimulation.
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