Event-related desynchronization of motor cortical oscillations in patients with multiple system atrophy
- PMID: 20821197
- DOI: 10.1007/s00221-010-2312-5
Event-related desynchronization of motor cortical oscillations in patients with multiple system atrophy
Abstract
Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by parkinsonism (MSA-P), cerebellar and autonomic deficits. In Parkinson's disease (PD), an impaired modulation of motor cortical mu and beta range oscillations may be related to the pathophysiology of bradykinesia. Event-related desynchronization (ERD) of these oscillations occur for 1-2 s preceding a voluntary movement in normal subjects and patients with PD treated with levodopa while only lasting around 0.5 s in untreated patients. Motor cortical rhythms were recorded from subdural strip electrodes in three patients with MSA-P while taking their regular dopaminergic medications. Following a ready cue, patients performed an externally cued wrist extension movement to a go cue. In addition, recordings were obtained during imagined wrist extension movements to the same cues and during self-paced wrist extensions. ERD and event-related synchronization were examined in subject-specific frequency bands. All patients showed movement-related ERD in subject-specific frequency bands below ~40 Hz in both externally cued and self-paced conditions. Preparatory ERD latency preceding self-cued movement was 900 ms in one patient and at or after movement onset in the other two patients. In the externally cued task, a short lasting (<1.3 s) ready cue-related ERD that was not sustained to movement onset was observed in two patients. Imagined movements resulted in go cue-related ERD with a smaller magnitude in the same two patients. These results indicate that the modulation of motor cortical oscillations in patients with MSA that are treated with levodopa is similar to that occurring in untreated patients with PD. The findings suggest that cortical activation in patients with MSA is diminished, may be related to pathophysiological changes occurring in the basal ganglia and correlates with the poor clinical response that these patients typically obtain with dopaminergic therapy.
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