Altered Cortical Network Dynamics during Observing and Preparing Action in Patients with Corticobasal Syndrome

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Abstract

Besides parkinsonism, higher order cortical dysfunctions such as apraxia are hallmarks of the corticobasal syndrome (CBS). To date, little is known about the electrophysiological underpinnings of these symptoms.

To shed more light on the pathophysiology of CBS, we recorded the magnetoencephalogram of 17 CBS patients and 20 age-matched controls engaged in an observe-to-imitate task. The task involved the display of a tool-use video in first person view (action observation), a written instruction to withhold movement until the presentation of a Go cue (movement preparation), and unilateral tool-use imitation. We investigated modulations of spectral power on the source level.

Action observation was associated with an event-related desynchronization in the beta-band (13-30Hz), which was weaker in CBS patients than in healthy controls. The group effect localized to superior parietal, primary motor, premotor and inferior frontal cortex bilaterally. While participants awaited the Go cue, beta power was again suppressed in the hemisphere contralateral to movement, and the rate of suppression correlated with reaction time. This modulation, too, was weaker in the CBS group. Immediately before movement onset, however, beta power was similar in both groups.

Our results reveal that action observation triggers beta suppression, likely reflecting motor cortical disinhibition, which is reduced in CBS patients. This pathological alteration might be a neural correlate of a selective deficit in the embedding of observed action into a motor representation (visuo-motor mapping). The suboptimal timing of the beta-power suppression to the upcoming Go cue presumably reflects a deficit in learning the trial’s temporal structure rather than a deficit in movement initialization.

Highlights

  • Action observation elicits a suppression of cortical beta power.

  • This suppression is diminished in CBS patients relative to controls.

  • The timing of beta desynchronization to an upcoming Go cue is impaired in CBS patients.

  • No evidence for an alteration of movement initialization in CBS patients.

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