Background: We monitor brain activities in thalamotomy for Parkinson's disease by a bipolar concentric microelectrode. Aim: The present study aimed to standardize the quantitative monitoring for targeting and for pathophysiological analysis. Methods: To show the process of data analysis, we selected 20 patients who gave informed consent for thalamotomy. The cases were divided into group I with rigidity, but no tremor (n = 10), and the group II with rigidity and tremor (n = 10). Most patients suffered from bradykinesia. We monitored the electromyograms of the neck and limb muscles. Brain activities were sampled as the electrode passed through the caudate and thalamic nuclei, divided into filtered local field potentials and multiple unit spikes, and rated at different depths by the summed periods in percent occupied by the component wavelets of field potentials at 3-7, 7-13, 13-27 and 27-80 Hz. Results: Analysis was summarized by the depth distribution histograms of dominant wavelet compositions. The 13-27-Hz activities were exaggerated in the caudate, thalamic ventroanterior and ventrolateral nuclei. The 3-7-Hz activities timelocked with tremor were exaggerated in the nucleus ventralis intermedius. Group I cases showed little 3-7-Hz activities. Thermolesion in the thalamus with those highly-rated activities alleviated tremor and rigidity, but spared most bradykinesia. Conclusion:The standardized analysis suggests that the thalamic 3-7-Hz and 13-27-Hz activities serve as the quantitative markers of pathophysiology representing tremor and rigidity, respectively.

Background: Parkinsonian rigidity is alleviated by thalamotomy targeting the thalamic nucleus ventralis lateralis. Detecting there the exaggerated 13-27-Hz b-band activities, we hypothesized that these activities centrally drove rigidity. Aim: To test this hypothesis, we examined the temporal relationships of rigidity with b-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 b-band activities when the thalamic recording sites somatotopically met the muscles of interest. The b-band activities consisted of the negative-going deflection of local field potentials and negativity-dominant multiple unit spikes. The b-band local field potentials led to the muscle spikes in spontaneous initiation and development of rigidity, as well as in the cyclic sequence of b-band activities and electromyograms. The paired b-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 b-band local field potentials and muscle spikes occurred contingently. When the b-band and tremor-locked 3-7-Hz s-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 b-band hyperactivities contingently drive rigidity in support for the central origin hypothesis of rigidity.

Background and Aim Passive and active muscle manipulations modify parkinsonian tremor and rigidity. We hypothesized that these outer maneuvers provoke thalamic 3 to 7‐Hz (τ‐range) and 13 to 27‐Hz (β‐band) activities, which in turn act to develop and maintain the symptoms. To test the hypothesis, we examined the temporal and quantitative relationships of the thalamic activities with the symptoms in conditions under the outer maneuvers. Methods In thalamotomy for 20 patients with Parkinson's disease, we monitored thalamic local field potentials and multiple unit spikes with surface electromyograms of neck and limb muscles. Results Tremor is intensified in postural and kinetic modes with higher amplitude and faster frequency than the resting state, and in tremor rhythms on the cogwheel rigidity with accelerated muscle tone. Exaggerated thalamic τ‐range activities always led to tremor of those intensified modes. The τ‐range activities developed and maintained tremor in keeping a quantitative relationship in amplitude. Both the passive and active muscle manipulations transiently abolished the β‐band activities, and then made them relapse to lead to rigidity in a waning and waxing fashion. Because of these changes of β‐band activities, the patient's active effort to move or hold postures caused a state in conflict between voluntary and involuntary contractions. Conclusion Together, the results suggest that passively activated peripheral kinesthetic afferents, and actively triggered central motor initiatives act to develop and maintain tremor and rigidity through the thalamic motor nuclei as the crucial relay stations.

Causes of death, with special reference to cerebral haemorrhage, among 240 patients with pathologically verified Parkinson's disease were investigated using the Annuals of the Pathological Autopsy Cases in Japan from 1981 to 1985. The leading causes of death were pneumonia and bronchitis (44.1%), malignant neoplasms (11.6%), heart diseases (4.1%), cerebral infarction (3.7%) and septicaemia (3.3%). Cerebral haemorrhage was the 11th most frequent cause of death, accounting for only 0.8% of deaths among the patients, whereas it was the 5th most common cause of death among the Japanese general population in 1985. The low incidence of cerebral haemorrhage as a cause of death in patients with Parkinson's disease may reflect the hypotensive effect of levodopa and a hypotensive mechanism due to reduced noradrenaline levels in the parkinsonian brain.