A dissociation between stopping and switching actions following a lesion of the pre-supplementary motor area

AbstractIntroductionAlthough the pre-supplementary motor area (pre-SMA) is one of the most frequently reported areas of activation in functional imaging studies, the role of this brain region in cognition is still a matter of intense debate. Here we present a patient with a focal lesion of caudal pre-SMA who displays a selective deficit in updating a response plan to switch actions, but shows no impairment when required to withhold a response – stopping.Materials & methodsThe patient and a control group underwent three tasks designed to measure different aspects of cognitive control and executive function.ResultsThe pre-SMA patient displayed no impairment when responding in the face of distracting stimuli (Eriksen flanker paradigm), or when required to halt an on-going response (STOP task). However, a specific deficit was observed when she was required to rapidly switch between response plans (CHANGE task).ConclusionsThese findings suggest that the caudal pre-SMA may have a particularly important role in a network of brain regions required for rapidly updating and implementing response plans. The lack of any significant impairment on other measures of cognitive control suggests that this is not likely due to a global deficit in cognitive control. We discuss the implications of these results in the context of current theories of pre-SMA function

Masked primes evoke partial motor responses

Backward-masked primes presented outside conscious awareness can affect responses to subsequently presented target stimuli. Differences in response times have been used to infer a pattern of sub-threshold activation and subsequent inhibition of motor plans associated with the primes. However, it is unclear whether competition between alternative responses is fully resolved in the brain or whether activated responses can begin being executed before the final decision to act has been made. Here, we investigate the dynamics of responses evoked by masked primes using a continuous measure – voltage change in force-sensing resistors simultaneously in both hands. Masked primes produced the predicted pattern of motor activation and subsequent inhibition of the primed response. There is no evidence that the effects of masked primes interact with spatial compatibility (e.g., Simon) effects, suggesting separate mechanisms underpinning these effects. Moreover, masked primes evoked partial motor decisions – measurable at the effectors as small amounts of erroneous response – which were usually rapidly corrected. Together, these errors and fast corrections question the ‘sub-threshold’ nature of responses evoked by masked primes and provide important constraints on models of decision-making

Longitudinal development of visual working memory precision in childhood and early adolescence

© 2016. Visual working memory (VWM) is the ability to hold in mind visual information for brief periods of time. The current study investigated VWM precision development longitudinally. Participants (N = 40, aged 7-11 years) completed delayed reproduction sequential VWM tasks at baseline and two years later. Results show age-related improvement in recall precision on both 1-item and 3-item VWM tasks, suggesting development during childhood and early adolescence in the resolution with which both single and multiple items are stored in VWM. Probabilistic modelling of response distribution data suggests age-related improvement in precision is attributable to a specific decrease in the variability (noisiness) of stored feature representations. This highlights a novel developmental mechanism which may underlie longitudinal improvement in VWM performance, crucially without invoking improvement in the number of items that can be stored. VWM precision provides a sensitive metric with which to track developmental changes longitudinally, shedding light on underlying cognitive mechanisms

The role of the ventrolateral frontal cortex in inhibitory oculomotor control

It has been proposed that the inferior/ventrolateral frontal cortex plays a critical role in the inhibitory control of action during cognitive tasks.However, the contribution of this region to the control of eye movements has not been clearly established.Here, we describe the performance of a group of 23 frontal lobe damaged patients in an oculomotor rule switching task for which the association between a centrally presented visual cue and the direction of a saccade could change from trial to trial. A subset of 16 patients also completed the standard antisaccade task.Ventrolateral damage was found to be a significant predictor of errors in both tasks. Analysis of the rate at which patients corrected errors in the rule switching task also revealed an important dissociation between left and right hemisphere damaged patients.Whilst patients with left ventrolateral damage usually corrected response errors with secondary saccades, those with right hemisphere lesions often failed to do so. The results suggest that the inferior frontal cortex forms part of a wider frontal network mediating inhibitory control over stimulus elicited eye movements. The critical role played by the right ventrolateral region in cognitive tasks may arise due to an additional functional specialization for the monitoring and updating of task rules

Automatic motor activation in the executive control of action

Although executive control and automatic behavior have often been considered separate and distinct processes, there is strong emerging and convergent evidence that they may in fact be intricately interlinked. In this review, we draw together evidence showing that visual stimuli cause automatic and unconscious motor activation, and how this in turn has implications for executive control. We discuss object affordances, alien limb syndrome, the visual grasp reflex, subliminal priming, and subliminal triggering of attentional orienting. Consideration of these findings suggests automatic motor activation might form an intrinsic part of all behavior, rather than being categorically different from voluntary actions

Brain mechanisms underlying apathy

The past few decades have seen growing interest in the neuropsychiatric syndrome of apathy, conceptualised as a loss of motivation manifesting as a reduction of goal-directed behaviour. Apathy occurs frequently, and with substantial impact on quality of life, in a broad range of neurological and psychiatric conditions. Apathy is also consistently associated with neuroimaging changes in specific medial frontal cortex and subcortical structures, suggesting that disruption of a common systems-level mechanism may underlie its development, irrespective of the condition that causes it. In parallel with this growing recognition of the clinical importance of apathy, significant advances have been made in understanding normal motivated behaviour in humans and animals. These developments have occurred at several different conceptual levels, from work linking neural structures and neuromodulatory systems to specific aspects of motivated behaviour, to higher order computational models that aim to unite these findings within frameworks for normal goal-directed behaviour. In this review we develop a conceptual framework for understanding pathological apathy based on this current understanding of normal motivated behaviour. We first introduce prominent theories of motivated behaviour-which often involves sequences of actions towards a goal that needs to be maintained across time. Next, we outline the behavioural effects of disrupting these processes in animal models, highlighting the specific effects of these manipulations on different components of motivated behaviour. Finally, we relate these findings to clinical apathy, demonstrating the homologies between this basic neuroscience work and emerging behavioural and physiological evidence from patient studies of this syndrome

Bihemispheric transcranial direct current stimulation enhances effector-independent representations of motor synergy and sequence learning.

Complex manual tasks-everything from buttoning up a shirt to playing the piano-fundamentally involve two components: (1) generating specific patterns of muscle activity (here, termed synergies ); and (2) stringing these into purposeful sequences. Although transcranial direct current stimulation (tDCS) of the primary motor cortex (M1) has been found to increase the learning of motor sequences, it is unknown whether it can similarly facilitate motor synergy learning. Here, we determined the effects of tDCS on the learning of motor synergies using a novel hand configuration task that required the production of difficult muscular activation patterns. Bihemispheric tDCS was applied to M1 of healthy, right-handed human participants during 4 d of repetitive left-hand configuration training in a double-blind design. tDCS augmented synergy learning, leading subsequently to faster and more synchronized execution. This effect persisted for at least 4 weeks after training. Qualitatively similar tDCS-associated improvements occurred during training of finger sequences in a separate subject cohort. We additionally determined whether tDCS only improved the acquisition of motor memories for specific synergies/sequences or whether it also facilitated more general parts of the motor representations, which could be transferred to novel movements. Critically, we observed that tDCS effects generalized to untrained hand configurations and untrained finger sequences (i.e., were nonspecific), as well as to the untrained hand (i.e., were effector-independent). Hence, bihemispheric tDCS may be a promising adjunct to neurorehabilitative training regimes, in which broad transfer to everyday tasks is highly desirable

Flexibility of representational states in working memory

The relationship between working memory (WM) and attention is a highly interdependent one, with evidence that attention determines the state in which items in WM are retained. Through focusing of attention, an item might be held in a more prioritized state, commonly termed as the focus of attention (FOA). The remaining items, although still retrievable, are considered to be in a different representational state. One means to bring an item into the FOA is to use retrospective cues (‘retro-cues’) which direct attention to one of the objects retained in WM. Alternatively, an item can enter a privileged state once attention is directed towards it through bottom-up influences (e.g. recency effect) or by performing an action on one of the retained items (‘incidental’ cueing). In all these cases, the item in the FOA is recalled with better accuracy compared to the other items in WM. Far less is known about the nature of the other items in WM and whether they can be flexibly manipulated in and out of the FOA. We present data from three types of experiments as well as transcranial magnetic stimulation to early visual cortex to manipulate the item inside FOA. Taken together, our results suggest that the context in which items are retained in WM matters. When an item remains behaviourally relevant, despite not being inside the FOA, re-focusing attention upon it can increase its recall precision. This suggests that a non-FOA item can be held in a state in which it can be later retrieved. However, if an item is rendered behaviourally unimportant because it is very unlikely to be probed, it cannot be brought back into the FOA, nor recalled with high precision. Under such conditions, some information appears to be irretrievably lost from WM. These findings, obtained from several different methods, demonstrate quite considerable flexibility with which items in WM can be represented depending upon context. They have important consequences for emerging state-dependent models of WM

Attention deficits following ADEM ameliorated by guanfacine

The authors report here the case of a patient with severe deficits in arousal and sustained attention, associated with hemispatial neglect. These impairments were secondary to acute disseminated encephalomyelitis, with bilateral involvement of the medial nuclei and pulvinar of the thalamus. Treatment with the noradrenergic agonist guanfacine, previously used for attention deficits in attention deficit/hyperactivity disorder and stroke, was associated with a significant amelioration of both the spatial and sustained attention impairments in neglect. Guanfacine may prove to be a useful tool in the treatment of disorders of attention associated with neurological conditions

Mechanisms Underlying Motivational Dysfunction in Schizophrenia.

Negative symptoms are a debilitating feature of schizophrenia which are often resistant to pharmacological intervention. The mechanisms underlying them remain poorly understood, and diagnostic methods rely on phenotyping through validated questionnaires. Deeper endo-phenotyping is likely to be necessary in order to improve current understanding. In the last decade, valuable behavioural insights have been gained through the use of effort-based decision making (EBDM) tasks. These have highlighted impairments in reward-related processing in schizophrenia, particularly associated with negative symptom severity. Neuroimaging investigations have related these changes to dysfunction within specific brain networks including the ventral striatum (VS) and frontal brain regions. Here, we review the behavioural and neural evidence associated with negative symptoms, shedding light on potential underlying mechanisms and future therapeutic possibilities. Findings in the literature suggest that schizophrenia is characterised by impaired reward based learning and action selection, despite preserved hedonic responses. Associations between amotivation and reward-processing deficits have not always been clear, and may be mediated by factors including cognitive dysfunction or dysfunctional or self-defeatist beliefs. Successful endo-phenotyping of negative symptoms as a function of objective behavioural and neural measurements is crucial in advancing our understanding of this complex syndrome. Additionally, transdiagnostic research-leveraging findings from other brain disorders, including neurological ones-can shed valuable light on the possible common origins of motivation disorders across diseases and has important implications for future treatment development