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Relationship between oscillations in the basal ganglia and synchronization of cortical activity Volume 4, supplement 3, Supplement 3, December 2002


   
   Figure 1. Postulated mechanism for the generation of rhythmic modulations of firing rate in the basal ganglia output nuclei. The cortical rhythm is propagated to the striatum, where it produces a rhythmic fluctuation in the membrane potential of striatal projection neurons. When the nigrostriatal system is intact, membrane potential fluctuation are under the threshold of action potential (left). In animals having nigrostriatal lesions, striatal projection neurons are more depolarised and a bursting activity appears leading to a bursting activity of SNR neurons (from Tseng et al., 2001 with permission).



   
   Figure 2. Neuronal acitivity in the STN of control rats (upper A): bursting activity of STN neurons is synchronized to cortical oscillation (EEG). This synchronization disappeared after ipsilateral cortical ablation (upper B). In 6OH dopamine-lesioned animals, there is an increase of bursting activity of STN neurons still correlated to cortical oscillation (lower A). After cortical ablation, STN neurons develop a tonic pattern discharge of firing rate (lower B). From Magill et al., 2001, with permission).



   
   Figure 3. Multiple electrode recordings in the globus pallidus of normal (A) and parkinsonian (B) monkeys. A: the upper trace shows a Òhigh frequency dischage with pausesÓ firing pattern typical of GPE cells. The two lower traces show high frequency discharge units of the GPI. B: GPI neurons exhibit intermittent episodes of synchronous periodic bursting (from Bergman et al., 1998, with permission).



   
   Figure 4. Microrecordings of STN neurons in parkinsonian patients. A: raw trace of a well isolated STN neuron with an oscillatory behavior. C-E: examples of autocorrelograms and frequency spectra for three types of oscillatory STN neurons. C: STN neuron with only a tremor frequency component. D: STN neuron with only a high frequency oscillatory component. E: STN neuron displaying both oscillatory components (from Levy et al., 2000, with permission).



   
   Figure 5. Cortico-muscular coherence of the Piper rhythm. Coherence spectrum between an magnetoencephalographic channel over the contralateral rolandic cortex and EMG of right forearm extensors during maximal isometric contraction, displaying a peak around 40-50 Hz (from Brown et al., 1998, with permission).



   
   Figure 6. Influence of GPI stimulation on force and EMG spectra in parkinsonian patients. A: Peak torque and forearm extensor EMG are improved by stimulation. B: Expanded section of the unrectified surface EMG in A. The pattern of EMG discharge changes from a 12 Hz action tremor to a Piper rhythm of 45 Hz when maximal contraction is performed during stmulation. C: Amplitude spectra of the rectified EMG recorded during sustained contraction. Without stimulation, muscle activity is dominated by oscillations at 12 Hz. This rhythm is suppressed during stimulation, and a new peak appears, centred on 45 Hz (from Brown, 2000, with permission).



   
   Figure 7. Inter-relationships between cortex, STN and muscle during tonic wrist extension in a parkinsonian patient. A: raw data of the simultaneously recorded EEG (upper trace), EMG of wrist extensors (lower trace) and pairs of contacts of the STN macroelectrode (three middle traces). B-D: autospectra of left rectified wrist EMG (B), right STN macroelectrode (C) and Cz-FCz (D). E-G: coherence spectra between rectified wrist extensor EMG and STN macroelectrode (E), STN macroelectrode and Cz-FCz (F), and rectified EMG and Cz-FCz (G) (from Marsden et al., 2001, with permission).



   
   Figure 8. Sensitivity to movement of STN oscillations. Recording of LFPs from an STN macroelectrode in a parkinsonian patient who is clenching his contralateral fist. STN oscillations decrease in amplitude a few hundreds ms before the onset of muscular activation, presumably demonstrating their role in movement preparation. This attenuation still persists during muscular activation. The lower trace is the EMG of the extensor carpi radialis muscle. The two upper traces are the signals of adjacent contacts of the STN macroelectrode.



   
   Figure 9. Influence of GPI stimulation on the spatiotemporal pattern of cortical reactivity ((rhythm) during voluntary movement. Mapping between - 1 500 ms before movement (movement execution at 0 s) and 1 000 ms after movement. A. Stimulation off and without L-dopa. B. Stimulation on without L-dopa. C. Stimulation on and L-dopa. Mapping of desynchronization of (rhythm from 13 electrodes is represented by warm colours.



   
   Figure 10. influence of STN stimulation on the spatiotemporal pattern of cortical reactivity ((rhythm) during voluntary movement. Mapping between - 1 500 ms before movement (movement execution at 0 s) and 1 000 ms after movement. A. Stimulation off and without L-dopa. B. Stimulation on, without L-dopa. C. Stimulation on and L-dopa. Mapping of desynchronization of the µ rhythm from 21 electrodes is represented by warm colours.