Sense of agency as synecdoche: Multiple neurobiological mechanisms may underlie the phenomenon summarized as sense of agency.

Functional magnetic resonance imaging (fMRI) studies on the sense of agency (SoA) have yielded heterogeneous findings identifying regional brain activity during tasks that probed SoA. In this review, we argue that the reason behind this between-study heterogeneity is a "synecdochic" way the field conceptualizes and studies SoA. Typically, a single feature is experimentally manipulated and then this is interpreted as covering all aspects of SoA. The purpose of this paper is to give an overview of the fMRI studies of SoA and attempt to provide meaningful categories whereby the heterogeneous findings may be classified. This classification is based on a separation of the experimental paradigms (Feedback Manipulations of ongoing movements, Action-Effect, and Sensory Attenuation) and type of report employed (implicit, explicit reports of graded or dichotic nature, and whether these concern self-other distinctions or sense of control). We only find that Feedback Manipulation and Action-Effect share common activation in supplementary motor area, insula and cerebellum in positive SoA and inferior frontal gyrus in the negative SoA, but observe large networks related to SoA only in Feedback Manipulation studies. To illustrate the advantages of this approach, we discuss the findings from an fMRI study which we conducted, within this framework.

On Denny-Brown's 'spastic dystonia' - What is it and what causes it?

In this review, we will work around two simple definitions of two different entities, which most often co-exist in patients with lesions to central motor pathways: Spasticity is "Enhanced excitability of velocity-dependent responses to phasic stretch at rest", which will not be the subject of this review, while Spastic dystonia is tonic, chronic, involuntary muscle contraction in the absence of any stretch or any voluntary command (Gracies, 2005). Spastic dystonia is a much less well understood entity that will be the subject this review. Denny-Brown (1966) observed involuntary sustained muscle activity in monkeys with lesions restricted to the motor cortices . He further observed that such involuntary muscle activity persisted following abolition of sensory input to the spinal cord and concluded that a central mechanism rather than exaggerated stretch reflex activity had to be involved. He coined the term spastic dystonia to describe this involuntary tonic activity in the context of otherwise exaggerated stretch reflexes. Sustained involuntary muscle activity in the absence of any stretch or any voluntary command contributes to burdensome and disabling body deformities in patients with spastic paresis. Yet, little has been done since Denny-Brown's studies to determine the pathophysiology of this non- stretch or effort related sustained involuntary muscle activity following motor lesions and there is a clear need for research studies in order to improve current therapy. The purpose of the present review is to discuss some of the possible mechanisms that may be involved in the hope that this may guide future research. We discuss the existence of persistent inward currents in spinal motoneurones and present the evidence that the channels involved may be upregulated following central motor lesions. We also discuss a possible contribution from alterations in synaptic inputs from surviving or abnormally branched sensory and descending fibres leading to over-activity and lack of motor coordination. We finally discuss evidence of alterations in motor cortical representational maps and basal ganglia lesions.

Motoneuronal drive during human walking.

Recent technical advances have made it possible to reveal some of the inputs that drive spinal motoneurones during normal human walking. These techniques are based either on a temporary removal of the drive to the motoneurones or on an analysis of the coupling of motor unit activity. During walking a sudden unloading of the plantarflexor muscles leads to a pronounced drop in the soleus EMG activity. This unloading effect is caused by cessation of activity in the sensory afferents, which mediate positive feedback from the active muscles in the stance phase. Somewhat surprisingly the drop in EMG activity following unloading is still observed when Ia afferents are blocked, suggesting that these afferents do not make an important contribution to the motoneuronal drive. It would seem that gr. Ib and/or gr. II afferents are the main contributors to the positive feedback. It has been known for a long time that transcranial magnetic stimulation (TMS) at low intensities may selectively activate local inhibitory circuits in the cortex. At such low intensities TMS applied over the motor cortex may thus inhibit the output from the cortex. The removal of the corticospinal drive in this way may be revealed as a drop in EMG activity from the active muscle. During walking TMS may evoke such a drop in EMG activity from the active muscles, which demonstrates that the corticospinal tract makes a contribution to the muscle activity. Time- and frequency domain analysis of motor unit activity have been shown to be effective tools in the analysis of synaptic drive to spinal motoneurones during tonic voluntary contraction. Applying these techniques to human walking reveals that motor units recorded from the same muscle or from close synergists show short-term synchrony and coherence in the 15-20 Hz frequency band. However, motor units from muscles acting at different joints show no coupling. This suggests that leg muscles are generally activated relatively independently of each other during human walking. These techniques show great promises for revealing changes in the sensory and corticospinal drive to motoneurones in relation to different tasks as well as in patients after injury to the central motor system.