In order to describe the thalamic data more accurately we next classified neurons by location into those in Vim versus Vop. The Vim mean rates were significantly greater in postural Angiogenesis inhibitor ET than in cerebellar tremor (P<0.01, shown in Fig. 2A), but not different from intention ET or from controls with pain (not shown). The mean Vim firing rate for intention ET was not significantly different from cerebellar tremor (not shown). The Vop mean rates of subjects with postural ET were higher than in cerebellar tremor (P=0.002, not shown). Therefore, firing rates in
postural ET were consistently higher than those in cerebellar tremor. The activity of all neurons included was studied for a response to joint movements during mapping of the thalamus, as described in the Methods. These cells were located in the region anterior ( Fig. 1C: P2) and dorsal to the region in which cells respond to cutaneous stimuli
( Fig. 1C: P1, and Lenz et al. (1988)). The proportions of cells responding to deep sensory stimuli and those not responding to such stimuli are shown by tremor type in Table 2. The proportion of neurons in Vim responding was greater for postural ET than cerebellar tremor (P=0.00012, Chi square with Bonferroni correction) and controls with pain (P=0.048). The number of sensory cells in Vop was different only between intention ET and cerebellar tremor (P=0.02, Fisher with Bonferroni). Since sensory inputs may be an important factor in the relationship of cerebellar tremor and cortical Trametinib purchase activity (Flament et al., 1984, Hore and Flament, 1986 and Vilis and Hore, 1977), we next examined the mean spontaneous rates for sensory cells across the four groups (Fig. 2B). There was a clear and significant change in the firing rate of sensory cells according to patient groups (1-way ANOVA, F=3.47, P<0.05). Post-hoc testing showed that the firing rate of sensory cells in the postural ET group was significantly higher than that of cerebellar tremor and controls with pain. The
rate for intention ET was not different from postural ET. We next examined how the thalamic signal qualitatively differed between groups of patients. The frequency at which peak spike activity G protein-coupled receptor kinase occurred was found for each neuron within the tremor range (1.9–7 Hz) (Lenz et al., 2002). The mean “frequency of peak spike power” occurred at a different frequency for each group of tremor patients (1-way ANOVA, F(3,259)=8.75, P<0.0005). The mean frequency of this peak is significantly higher in postural ET patients (4.8 Hz+0.25, mean+SEM) as compared to cerebellar tremor (3.4 Hz+0.2, post-hoc Newman–Keuls test, P=0.0057) and intention ET (3.7 Hz+0.4, P=0.032). The frequency was not significantly different between intention ET and cerebellar tremor (Newman–Keuls test P=0.34).