Central origin of parkinsonian rigidity examined with thalamic activities on their temporal relationships

Background Parkinsonian rigidity is alleviated by thalamotomy targeting the thalamic nucleus ventralis lateralis. Detecting there the exaggerated 13–27-Hz β-band activities, we hypothesized that these activities centrally drove rigidity. Aim To test this hypothesis, we examined the temporal relationships of rigidity with β-band activities. Methods In 20 patients with Parkinson's disease, we monitored the thalamic local field potentials and multiple unit spikes with the electromyograms of neck and limb muscles. Results The resting state of muscles with exaggerated tonic discharges in electromyograms was regarded to represent rigidity. The compound muscle spikes as such were accompanied by or synchronized with the thalamic β-band activities when the thalamic recording sites somatotopically met the muscles of interest. The β-band activities consisted of the negative-going deflection of local field potentials and negativity-dominant multiple unit spikes. The β-band local field potentials led to the muscle spikes in spontaneous initiation and development of rigidity, as well as in the cyclic sequence of β-band activities and electromyograms. The paired β-band local field potentials and muscle spikes were moderately correlated in amplitude. During the observation, the grade of rigidity spontaneously fluctuated. Accordingly, the phase coincidence of β-band local field potentials and muscle spikes occurred contingently. When the β-band and tremor-locked 3–7-Hz τ-range activities coexisted at the recording site, different groups of thalamic neurons led to rigidity and tremor, respectively, as their peripheral outcomes. Conclusion The results suggest that the thalamic β-band hyperactivities contingently drive rigidity in support for the central origin hypothesis of rigidity.