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Modulations of beta oscillatory power serve a predictive role, in preparation of future actions. It is well known that beta amplitude decreases prior to voluntary movements and expected tactile stimuli. Paradoxically, recent studies have reported a beta amplitude increase prior to expected visual and auditory stimuli. Moreover, it has been suggested that, in isochronic stimulus series, the rising beta slope is adjusted to the duration of the interstimulus interval. We investigated the characteristics of such timing related pre-stimulus beta power increases using visual stimulus sequences that were presented at three regular rates (0.61, 0.74 and 0.95Hz). EEG was recorded from twenty participants while they attended the sequences by performing a clock reading task. Time-frequency analyses showed a consistent pattern of beta modulation: the post-stimulus beta power decrease was followed by a steep increase. Contrary to recent views, we found that the peaks of beta power, for the three presentation rates, were reached at a similar latency post-stimulus, instead of a fixed interval preceding the next stimulus. This demonstrates that, at interstimulus intervals between 1–2s, beta synchronization slopes are not modulated by timing mechanisms related to prediction of upcoming stimuli. We reconcile the discrepant results by proposing that when shorter interval durations are used, as in previous studies, beta resynchronization is interrupted by the presentation of a new stimulus, making it seem as if beta power peaks prior to upcoming stimuli. We emphasize caution with respect to the notion that the timing of beta synchronization is an expression of predictive timing.

While slowness of movement is an obligatory characteristic of Parkinson’s disease (PD), there are conditions in which patients move uncharacteristically fast, attributed to deficient motor inhibition. Here we investigate deficient inhibition in an optimal sensory-motor integration framework, using a game in which subjects used a paddle to catch a virtual ball. Display of the ball was extinguished as soon as the catching movement started, segregating the task into a sensing and acting phase. We analyzed the behavior of 9 PD patients (ON medication) and 10 age-matched controls (HC). The switching times (between sensing and acting phase) were compared to the predicted optimal switching time, based on the individual estimates of sensory and motor uncertainties. The comparison showed that deviation from predicted optimal switching times were similar between groups. However, PD patients showed a weaker correlation between variability in switching time and sensory-motor uncertainty, indicating a reduced propensity to generate exploratory behavior for optimizing goal-directed movements. Analysis of the movement kinematics revealed that PD patients, compared to controls, used a lower peak velocity of the paddle and intercepted the ball with greater velocity. Adjusting the trial duration to the time for the paddle to stop moving, we found that PD patients spent a smaller proportion of the trial duration for observing the ball. Altogether, the results do not show the premature movement initiation and truncated sensory processing that we predicted to ensue from deficient inhibition in PD.

Many sensorimotor activities have a time constraint for successful completion. In this case, any time devoted to sensory processing is at the expense of time available for motor execution. Earlier studies have explored how this competition between sensory processing and motor execution is resolved by using experimental designs that segregate the sensing and acting phase of the task. It was found that participants switch from the sensing to the acting stage such that the overall (sensorimotor) uncertainty in the outcome of the task is minimized. An unexplained observation in these studies is the substantial variability in switching times. We investigated the variability in switching time by correlating it with the underlying sensorimotor uncertainty. To this end, we used a modified version of the virtual ball catching paradigm proposed by Faisal & Wolpert (2009). Subjects were instructed to catch a ball, but as soon as they initiated their movement the ball disappeared. We extended the range of horizontal velocities and used two different start positions of the ball to quantify the dependence of sensory uncertainty on ball velocity. Velocity dependence of sensory uncertainty allowed us to manipulate sensory uncertainty and hence the sensorimotor uncertainty. We found that the variability in switching times is correlated with two factors. Firstly, variability in switching times is greater when variation in switching time has only minimal effects on sensorimotor uncertainty. Secondly, variability in switching times is greater when the sensorimotor uncertainty is larger. Our results suggest that the variability in switching time reflects an uncertainty-driven exploratory process.

In the Thatcher illusion, a face with inverted eyes and mouth looks abnormal when upright but not when inverted. Behavioral studies have shown that thatcherization of an upright face disrupts perceptual processing of the local configuration. We recorded high-density EEG from normal observers to study ERP correlates of the illusion during the perception of faces and nonface objects, to determine whether inversion and thatcherization affect similar neural mechanisms. Observers viewed faces and houses in four conditions (upright vs. inverted, and normal vs. thatcherized) while detecting an oddball category (chairs). Thatcherization delayed the N170 component over occipito-temporal cortex to faces, but not to houses. This modulation matched the illusion as it was larger for upright than inverted faces. The P1 over medial occipital regions was delayed by face inversion but unaffected by thatcherization. Finally, face thatcherization delayed P2 over occipito-temporal but not over parietal regions, while inversion affected P2 across categories. All effects involving thatcherization were face-specific. These results indicate that effects of face inversion and feature inversion (in thatcherized faces) can be distinguished on a functional as well as neural level, and that they affect configural processing of faces in different time windows.

The cerebral network associated with Holmes tremor has never been determined directly. A previous study reported a brain network that is functionally connected, in healthy individuals, to different lesions that cause Holmes tremor (lesion connectome). We report a 71‐year‐old man with severe left‐sided tremor caused by a microbleed near the right red nucleus. Using accelerometry‐fMRI, we show tremor‐related activity in contralateral sensorimotor cortex and cerebellar vermis. This network was distinct from, but functionally coupled to, the Holmes lesion connectome. We propose that Holmes tremor involves three distinct cerebral mechanisms: a structural lesion, an intermediate lesion connectome, and symptom‐related activity.

Brain imaging studies have implicated the basal ganglia in the scaling of movement velocity. Basal ganglia activation has also been reported for movement timing. We investigated the neural correlates of scaling of force and time in the production of rhythmic motor sequences using functional magnetic resonance imaging (fMRI) of the human brain. Participants ( N = 13) were imaged while squeezing a rigid force transducer in a near isometric manner between thumb and index finger, to reproduce four different rhythmic sequences. The responses were separated by either equal (600 ms) or alternating (400, 800 ms) intervals, and produced with either equal (12 N) or alternating (8, 16 N) forces pulses. Intervals and force levels were balanced across each condition. The primary motor cortex (M1), supplementary motor area (SMA), basal ganglia, thalamus, and cerebellum were activated during the production of sequences marked by equal interval and force. There was no reliable main effect of alternating interval. In contrast, greater activation of these regions was associated with the extra demands of responding with alternating force pulses. We interpret the data as identifying a significant role of the BG in the control of force. In addition, the results indicate the importance of monitoring force when studying brain activation associated with motor timing.

Neurophysiological studies in non-human primates have provided evidence for simultaneous activation of competing responses in the (pre)motor cortex. Human evidence, however, is limited, partly because experimental approaches have often mapped competing responses to paired effectors represented in opposite hemispheres, which restricts the analysis to between-hemisphere comparisons and allows simultaneous execution. A demonstration of competition between different movement plans in the motor cortex is more compelling when simultaneous execution of the alternative responses is ruled out and they are represented in one motor cortex. Therefore, in the current MEG study we have used a unimanual Eriksen flanker paradigm with alternative responses assigned to flexion and extension of the right index finger, activating different direction-sensitive neurons within the finger representation area of the same motor cortex. Results showed that for stimuli eliciting response competition the pre-response motor cortex beta-band (17–29Hz) power decreased stronger than for stimuli that did not induce response competition. Furthermore, response competition elicited an additional pre-response mid-frontal high-gamma band (60–90Hz) power increase. Finally, larger gamma-band effect sizes correlated with greater behavioral response delay induced by response competition. Taken together, our results provide evidence for co-activation of competing responses in the human brain, consistent with evidence from non-human primates. •Using MEG we investigated oscillatory correlates of response competition.•The unimanual flanker task implemented a strong test of competing activations.•Response competition was expressed by sensorimotor beta-power suppression.•Co-incident frontal gamma-power increase correlates with response slowing.•The results stimulate analyses of oscillatory activity in response selection.

Background Mutations of SCN8A encoding the neuronal voltage-gated sodium channel NaV1.6 are associated with early-infantile epileptic encephalopathy type 13 (EIEE13) and intellectual disability. Using clinical exome sequencing, we have detected three novel de novo SCN8A mutations in patients with intellectual disabilities, and variable clinical features including seizures in two patients. To determine the causality of these SCN8A mutations in the disease of those three patients, we aimed to study the (dys)function of the mutant sodium channels. Methods The functional consequences of the three SCN8A mutations were assessed using electrophysiological analyses in transfected cells. Genotype–phenotype correlations of these and other cases were related to the functional analyses. Results The first mutant displayed a 10 mV hyperpolarising shift in voltage dependence of activation (gain of function), the second did not form functional channels (loss of function), while the third mutation was functionally indistinguishable from the wildtype channel. Conclusions Comparison of the clinical features of these patients with those in the literature suggests that gain-of-function mutations are associated with severe EIEE, while heterozygous loss-of-function mutations cause intellectual disability with or without seizures. These data demonstrate that functional analysis of missense mutations detected by clinical exome sequencing, both inherited and de novo, is valuable for clinical interpretation in the age of massive parallel sequencing.

The 'attentional blink' (AB) reflects a limitation in the ability to identify multiple items in a stream of rapidly presented information. Repetitive transcranial magnetic stimulation (rTMS), applied to a site over the right posterior parietal cortex, reduced the magnitude of the AB to visual stimuli, whilst no effect of rTMS was found when stimulation took place at a control site. The data confirm that the posterior parietal cortex may play a critical role in temporal as well as spatial aspects of visual attention.