, 1999 and Schell and Strick, 1984), which is densely interconnected with the motor cortex (Tanji, 1994). Vim is reciprocally connected with motor cortex and Vop receives considerable input from these cortical motor structures

through the cortico–thalamic Belnacasan solubility dmso projection. These connections may explain why increased firing rates in postural tremor are found in both Vim and Vop (Hirai and Jones, 1989, Hua and Lenz, 2005 and Lenz et al., 2002). Spectral analysis showed that coherence and phase for intention ET were more similar to cerebellar tremor than to postural ET (Fig. 4 and Fig. 5). The phase lead was significantly greater for postural ET than for intention ET. Intention ET and cerebellar tremor patients had much lower coherence and SNR than

postural ET subjects. Overall, this physiology seems to confirm the clinical observation that intention ET is similar to cerebellar tremor (Brennan et al., 2002 and Elble and Koller, 1990). The frequency of peak spike power was higher for the postural ET group than for the intention ET or cerebellar tremor groups, which is consistent with the similarities noted above. Clinically, cerebellar tremor is of lower frequency than essential tremor (Elble, 2006 and Findley and Koller, 1987). The lower frequency of intention ET and cerebellar Cyclopamine supplier tremor versus postural ET again suggests that intention ET is more like cerebellar tremor than postural ET. Patient 4 was not an exceptional case since there was no bias in the sampling of cell types or predominance of a particular nuclear location. Patient 4 was indistinguishable from other patients in the intention ET group in terms of spontaneous firing rates, and frequency of peak spike power in the tremor range. If a pacemaker of the cerebellum and related systems drives intention ET then a lesion of the cerebellum might further reduce this patient’s tremor and would not increase tremor. In postural ET, lesions of the cerebellum PRKD3 or pontine cerebellar connections decrease tremor (Dupuis et al., 1989 and Nagaratnam and Kalasabail, 1997). Therefore, the increase in intention tremor following the cerebellar stroke

in patient 4 is consistent with a mechanism of intention ET related to disruption of the cerebellum rather than to a pacemaker (Destexhe and Sejnowski, 2001, Lenz et al., 1994b and Stein and Oguztoreli, 1976). This difference could be tested by imaging studies of basal- and tremor-evoked activity in patients with either postural ET or intention ET. The analysis of thalamic neuronal activity and of the spike×EMG cross-correlation demonstrates that intention ET is more like cerebellar tremor than like postural ET. Of course, cerebellar tremor is often associated with lesions of the cerebellum or its output pathways (Carrea and Mettler, 1947 and Gilman et al., 1976). Therefore, the present results suggest the intention ET is associated with disruption of the cerebellum, which may be consistent with the histologic changes in Essential Tremor (Louis et al.