Synchronisation in the beta band has been hypothesised to be essentially antikinetic in nature and pathophysiologically relevant to bradykinesia. This is supported by a number of observations relating changes in beta activity with behaviour and treatment. One of the earliest behavioural observations was that the beta LFP activity picked up in the subthalamic nucleus (STN) and globus palli-dus interna (GPi) was reduced in PD patients prior to and during self and externally paced voluntary movements (Cassidy et al., 2002). Indeed, the mean timing of the drop in activity following a cue to move positively correlates with the mean reaction time across patients, which it precedes (K€hn et al., 2004). This relationship is so strong it may even be observed in individual subjects across single trials (Williams et al., 2005). If the reduction in beta activity is linked specifically to the facilitation of subsequent movement, an augmentation of power might also be predicted in this frequency band when a pre-prepared movement requires cancellation. This has been confirmed in subthalamic recordings during the 'Go-NoGo' paradigm (Kuhn et al., 2004). In addition, a strong relationship between motor processing and beta suppression has been suggested by experiments that compare the suppression of beta activity following warning cues in reaction time tasks. These cues can be either fully informative or uninformative about the direction indicated by subsequent imperative cues eliciting movement with either the left or right hand. In the case of uninformative cues there is no prospective information about which hand will be called upon to move, so motor selection can only occur after the go cue, as confirmed by longer reaction times. Under these circumstances the suppression of the beta activity following the warning cue is far less than following an informative warning cue, indicating that the beta suppression related to the amount of motor preparation that was possible rather than to any nonspecific alerting effect of the warning cue (Williams et al., 2003).
Treatment related modulations of oscillatory activity
The earliest observation relating to beta band oscillations in BG LFPs in patients with PD was that they were increased after the withdrawal of levodopa and suppressed following its return (Fig. 1). Thus background levels of beta activity were increased as motor performance deteriorated in the off medication state. More recently, it has also become apparent that the relative degree of beta suppression prior to and during movement is diminished after PD patients have been withdrawn from levodopa (Doyle et al., 2005). The increase in background levels of beta and the decrease in the reactivity of beta oscillations prior to and during movement might contribute to the paucity and slowness of voluntary movements, respectively.
Of course another effective treatment for akinesia is high frequency deep brain stimulation (DBS). Here it has proven technically difficult to record beta activity during stimulation of the same site, but it has been possible to record beta activity from the GPi during stimulation of the subthalamic area in patients with PD. This has confirmed that
R STN OFF
R STN OFF
Fig. 1. Power spectra of LFP activity recorded from the contacts of a DBS electrode in the subthalamic nucleus of a patient with PD on and off their antiparkinsonian medication. Off medication, the LFP is dominated by oscillations with a frequency of around 20 Hz, in the so-called beta band. After treatment with levodopa there is suppression of the beta band activity and a new oscillation arises in the gamma band, - peaking at 75 Hz. Mains artefact at 50 Hz has been omitted
Fig. 1. Power spectra of LFP activity recorded from the contacts of a DBS electrode in the subthalamic nucleus of a patient with PD on and off their antiparkinsonian medication. Off medication, the LFP is dominated by oscillations with a frequency of around 20 Hz, in the so-called beta band. After treatment with levodopa there is suppression of the beta band activity and a new oscillation arises in the gamma band, - peaking at 75 Hz. Mains artefact at 50 Hz has been omitted high frequency DBS also suppresses background levels of beta activity, in tandem with clinical improvement (Brown et al., 2004).
Earlier, it was stressed that increased synchronisation in the beta frequency band was a characteristic of activity throughout the BG-cortical loop. Accordingly, the same relationship between beta synchrony and motor impairment would be anticipated at the level of the cerebral cortex in patients with PD. A recent study in patients with chronically implanted DBS electrodes found that the degree of synchronisation in the beta band between cortical sites over central motor areas correlated with motor impairment, when patients were withdrawn from medication and therapeutic stimulation. In addition, both the reduction in beta synchronisation effected by high frequency stimulation of the STN, and that achieved with levodopa, correlated with treatment induced improvements in motor performance (Silberstein et al., 2005a).
Finally, if beta activity is essentially anti-kinetic in nature, could its excessive suppression following antiparkinsonian therapy or lesioning of the STN help explain hyperkinesias? Recent recordings in the GP of PD patients during levodopa-induced dyskinesias demonstrate that dyskinetic muscle activity may inversely correlate with pallidal beta activity, in keeping with the latter's posited antikinetic character (Silberstein et al., 2005b).
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