Understanding changes in cerebral and cerebellar motor representation during long-term motor training might help to develop most effective training procedures. For brain damage after stroke, these neuroplastic processes are different than those observed in healthy volunteers. Several factors modify training progress and motor representation in these patients. This talk will summarize recent findings on these issues and will focus predominantly on upper limb motor training. [mehr]

Identical sensory stimulation results in highly dynamic response patterns in primary sensory cortex, despite the physical constancy of external factors. This response modulation is thought to be partly attributable to activity intrinsic to the brain itself, such as behavioral state and previous experience. Two prominent factors contributing to intrinsic brain activity are feedback signals from higher order areas and the history of coactivation amoung sensory cells. I will discuss a series of experiments that investigate the effects of cortical feedback and stimulus repetition on sensory coding in the primary visual cortex. We find that both feedback activity and sensory experience increase the amount of sensory information retrievable from population responses without changing the average activity of single cells or the mean activity across the population. Specifically, the information is encoded in the distributed pattern of activity across the population, as predicted by population coding and Hebbian plasticity. These findings suggest that early sensory cortices provide a highly flexible representation of external variables which reflects both the current state of higher order brain areas, as well as the history of previous stimulation. Time permitting, I will also discuss recent progress in our attempts to increase the spatial coverage of in vivo electrophysiology, while simultaneously acquiring signals at multiple spatial scales: from single neurons to whole brain areas. [mehr]

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Recovery from spinal cord injury – and its attendant neurodegenerative processes – can follow a complicated trajectory spanning several years after trauma, where the ensuing diaschisis (meaning "shocked throughout") affects the entire neuroaxis. With potential treatments targeting repair of the injured spinal cord, there is an imperative to improve clinical trial design and efficiency, optimise patient stratification in the context of disease heterogeneity and identify potential trial outcome measures. The ability to track trauma-induced structural changes across the neuroaxis provides the opportunity to quantify pathological processes driving diaschisis and recovery-related plasticity. During my talk I will present evidence of progressive volume and microstructural changes (myelin and iron content) following acute spinal cord injury using state-of-the-art computational anatomy and post-processing tools. Further I will show latest developments of high-resolution MRI sequences and optimized post-processing methods to assess at the voxel level spinal cord grey and white matter changes. Finally, I will outline an integrative framework, which attempts to identify subgroups of neurologic disorders beyond standard clinical phenotyping – and to improve functional outcome with individualized treatment (i.e., precision neurology). This framework, franchised under the term “Embodied Neurology”, pays special emphasis on the reciprocal information flow between the body, spinal cord and brain. Spinal cord injury is a particularly interesting model in the context of EN as a focal traumatic lesion in the spinal cord has far reaching consequences in terms of both cortical reorganization at distant sites (cf. functional diaschisis) and the functional architecture within and beyond the spinal cord (cf. structural diaschisis). To establish EN there is a pressing need for further developments in neuroimaging with the aim to unify structural and functional biophysical models in order to link pathology to phenomenology with greater precision. [mehr]

The efficacy of various neurotransmitter systems declines with advancing age. Of particular interest, various pre- and post-synaptic components of the frontal and striatal dopaminergic systems show substantial negative age-related differences across the adult life span. Furthermore, anatomical and functional changes in the frontal and hippocampal regions are also hallmarks of brain aging. This talk will selectively highlight findings from recent neuroimaging, pharmacological and genetic studies about aging of the frontal-hippocampal-striatal circuitry and the implications for memory, spatial learning, and sequential decision-making in old age. [mehr]

In Clinical Neurology, ataxia denotes a syndrome of motor incoordination that typically results from dysfunction of the cerebellum and its afferent and efferent connections. Ataxia is also used to denote a group of neurodegenerative diseases of the cerebellum and its connections that are clinically characterized by progressive motor incoordination. Many of the ataxias have genetic causes, but there are also sporadic degenerative ataxias and ataxias which are due to acquired non-genetic causes. Overall, there is an enormous degree of heterogeneity among the ataxias with an estimated number of more than 150 different, molecularly defined diseases. Our research is focusing on the common, autosomal dominantly inherited spinocerebellar ataxias (SCA) which are caused by translated CAG repeat expansion mutations that code for an elongated polyglutamine tract within the respective proteins. To define the phenotype and natural history of these disorders we recruited a cohort of more than 500 patients and followed them over more than 8 years. Multivariate models allowed to explain up to 60% of the variability of the ataxia severity at baseline. Modelling of disease progression revealed genotype-specific patterns and identified biological factors that determine the rate of progression. MRI studies showed progressive grey and white matter tissue loss in cerebellum, brainstem and basal ganglia. Studies of a cohort of more than 300 apparently healthy SCA mutation carriers showed that first signs of impaired coordination and tissue loss of the brainstem or cerebellum occur more than 10 years before the clinical onset of ataxia. These observation led to a refined disease model of ataxia disorders that considers ataxia as a late disease stage which is preceded by extended asymptomatic and preclinical disease stages that offer a time window for early therapeutic intervention. Although CAG repeat expansion mutations are now known for more than two decades the mechanism how these mutations cause neurodegeneration remain far from clear. There is one component which is due to the toxic properties of proteins or protein fragments that contain elongated polyglutamine tracts. However, there are additional components that depend on the protein context of the polyglutamine tract and are disease specific. Currently, there is no treatment for SCA. Experimental work in cells and animals aims to reduce levels of mutant proteins using RNA interference (RNAi)and antisense oligonucleotides (AONs). An alternative approach is protein modification through AON-mediated exon skipping. As there are many obstacles to translate these approaches into clinical application there is renewed interest in finding drugs that interfere with cerebellar neuronal activity and thereby symptomatically improve ataxia. [mehr]

Human decision making often involves weighting of values obtained via the rewarding quality of experience, but can uniquely incorporate more abstract aspects such as information about possible long-term consequences. While the former is computationally simple and efficient, the latter requires utilization of a model about the world. I will present results of two studies aiming to disentangle unique learning mechanisms for both propensities. The first will focus on the cortical temporal dynamics of learning from reward compared to information revealed in the human EEG. The second will focus on regional specificity of neural correlates of learning from model-free and model-based outcomes that dissociate ventral from dorsal striatum in the fMRI. [mehr]

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We all have our habits, good and bad. But only for some, habits go from bad to worse and behaviour becomes compulsive, as we see for example in addiction or clinical overeating. How is it that a useful mechanism such as our habit system can come to work against us? Why does it happen for only some and not others when faced with tempting rewards? And how can we get back in control? In my doctoral studies I aimed to increase our understanding of this by investigating the neural and cognitive mechanisms underlying compulsive gambling (in gambling addiction) and eating behaviour (in a non-clinical population). Building on an extensive body of addiction literature, I used a variety of experimental paradigms to tap into different aspects of compulsive behaviour. I focussed in particular on altered reward processing and loss of control over automatic tendencies triggered by reward-related stimuli. Furthermore, I investigated the effects of a pharmacological (dopamine) and a behavioural (mindfulness) intervention on reward processing. [mehr]

What makes our experience of music possible – and effortless – is an intricate puzzle of cognitive processes, involving a subtle interplay of what psychologists refer to as bottom-up and top-down components. The key concept of expectation can be construed at the centre of a complex feedback loop between these components, relaying information in both directions, and at different time scales. This framework holds not just for music we hear (an exogenous/bottom-up process) but also for music we create in our minds (endogenous/top-down). One mode of acquiring musical knowledge is implicit learning, which gradually gets to shape our sensory preferences, e.g. for certain combinations of simultaneous notes over others (consonant over dissonant chords – or indeed, in some contexts, vice-versa!), and also our unfolding expectations relating to e.g. what musical event might come next. These expectations form the core of a set of intuitions that have been formalised as models of musical structure, most notably Schenkerian analysis. Such models can inspire quantifiable predictions about the temporal nature of our expectation – for instance, with regards to the moment in time when we feel a piece is "beginning to end". The sum of these intuitions endows us with a template that on the one hand enables us to make sense of music that we hear; but equally, also to (re)create music in our own minds – a process known as musical imagery, which shares commonalities with music perception not only at the cognitive level (e.g. both can be conjectured to stem from a single generative model) but also at the neuronal level. In this talk, I will describe three distinct studies from the Dresden Music Cognition Lab, that address – using behavioural and neuroimaging methods – individual elements of the expectation-mediated loop outlined above, namely (i) the (local) perception of consonance and dissonance; (ii) the (non-local) perception of hierarchical musical structures; and (iii) the role of harmonic function in imagined music. I will then attempt to integrate these findings into the larger questions of how expectation guides our listening and imagery of music, and how the brain is wired to make these processes run smoothly in the background. Keywords: Musical imagery, Schenkerian analysis, consonance and dissonance; decoding fMRI, multivariate pattern analysis, time series analyses. [mehr]

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The neuropsychology of familiar people recognition through face and voice will be surveyed from the clinical and the cognitive point of view, taking into account modality-specific (prosopagnosia and phonagnosia) and multimodal person recognition disorders. Our starting assumption was that many patients with right temporal lobe atrophy are incorrectly labelled as prosopagnosics, because faces are often considered as the most important channel used to recognize familiar people. In fact a multimodal familiar person recognition disorder may more accurately characterise the deficit in these patients. The clinical and the cognitive implications of this starting point will be developed and some current research perspectives will be exposed. [mehr]

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