Subthalamic nucleus stimulation modulates motor cortex oscillatory activity in Parkinson's disease.

In Parkinson's disease, impaired motor preparation has been related to an increased latency in the appearance of movement-related desynchronization (MRD) throughout the contralateral primary sensorimotor (PSM) cortex. Internal globus pallidus (GPi) stimulation improved movement desynchronization over the PSM cortex during movement execution but failed to improve impaired motor preparation. PET studies indicate that subthalamic nucleus (STN) stimulation partly reverses the abnormal premotor pattern of brain activation during movement. By monitoring MRD, we aimed to assess changes in premotor and PSM cortex oscillatory activity induced by bilateral STN stimulation and to compare these changes with those induced by l-dopa. Ten Parkinson's disease patients and a group of healthy, age-matched controls performed self-paced wrist flexions in each of four conditions: without either stimulation or l-dopa (the 'off' condition), with stimulation and without l-dopa (On Stim), with l-dopa and without stimulation ('on drug'), and with both stimulation and l-dopa (On Both). Compared with the Off condition, in both the On Stim and the On Drug condition the Unified Parkinson's Disease Rating Scale (UPDRS) III score decreased by about 60% and in the On Both condition it decreased by 80%. The desynchronization latency over central regions contralateral to movement and the movement desynchronization over bilateral central regions were significantly increased by stimulation and by l-dopa, with a maximal effect when the two were associated. Furthermore, desynchronization latency significantly decreased over bilateral frontocentral regions in the three treatment conditions compared with the Off condition. In Parkinson's disease, STN stimulation may induce a change in abnormal cortical oscillatory activity patterns (similar to that produced by l-dopa) by decreasing the abnormal spreading of desynchronization over frontocentral regions and increasing PSM cortex activity during movement preparation and execution, with a correlated improvement in bradykinesia. Parkinsonians under treatment displayed a desynchronization pattern close to that seen in healthy, age-matched controls, although central latencies remained shorter. The study indicates that it is possible to influence cortical reactivity related to the planning and execution of voluntary movement through the basal ganglia, and furthermore that the oscillatory activity of the PSM cortex (in addition to that of premotor areas) could be of major importance in the control of movement-associated, neural activity in Parkinson's disease.

Intermuscular coherence in Parkinson's disease: relationship to bradykinesia.

We hypothesised that bradykinesia may be partly due to the failure of the corticomuscular system to engage in high frequency oscillatory activity in Parkinson's disease (PD). In healthy subjects such oscillations are evident in coherence between active muscles at 15--30 Hz. We therefore investigated the effects of therapeutic stimulation of the basal ganglia on this coherence and related it to changes in bradykinesia in the contralateral arm. Increases in coherence at 15--30 Hz and improvements in bradykinesia upon stimulation were correlated (r = 0.564, p < 0.001). This suggests that the basal ganglia modulate oscillatory activity in the corticomuscular system and that impairment of the motor system's ability to engage in synchronised oscillations at high frequency may contribute to bradykinesia in PD.

Thalamic tremor: correlations with three-dimensional magnetic resonance imaging data and pathophysiological mechanisms.

Tremor associated with a single focal thalamic lesion has rarely been reported. Furthermore, the exact localization of the lesions is difficult to determine because of the imprecision of "conventional" radiology (computed tomography scan and/or "standard" magnetic resonance imaging). The aim of this study was to identify which thalamic structures are involved in tremor associated with a single focal thalamic lesion. We selected two patients who presented with unilateral postural and kinetic tremor of the upper limb related to a localized thalamic infarction. Three-dimensional T1-weighted magnetic resonance imaging sequence (MP-RAGE sequence) was used to determine the precise topography of the lesions by stereotactic analysis using the atlas of Hassler. The lesions were located within the pulvinar, the sensory nuclei, the mediodorsal nucleus, and the ventral lateral posterior nucleus (according to the classification of Hirai and Jones), the latter including the ventral intermediate nucleus (Vim according to the classification of Hassler). However, the Vim was spared. The subthalamic area, which can induce tremor, was not involved. After having compared the topography of the lesions with the clinical findings, we suggest that thalamic tremors may result from the interruption of the cerebellar outflow tract to the Vim within the thalamus.