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Action decisions in health and Parkinson’s disease

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  • UserDr. James Rowe, Department of Clinical Neurosciences / MRC Cognition and Brain Sciences Unit
  • ClockWednesday 30 September 2009, 09:45-10:15
  • HouseWest Road Concert Hall.

If you have a question about this talk, please contact Hannah Critchlow.

This talk is part of the Cambridge Clinical Neuroscience and Mental Health Symposium, 29th – 30th September 2009 at West Road Concert Hall. This event is free to attend for cambridge neuroscientists although registration is required. To register, and for further information, please visit:

Abstract: Many neurological and psychiatric disorders affect volition, including disorders of motivation, selection, inhibition and execution of voluntary actions. Here, we focus on the problem of how we choose one action over other possible actions when environmental cues (stimuli) and rewards (learned outcomes) do not provide sufficient information for a preferred choice. We show how a race model between competitive response schemas can be used to inform the analysis of fMRI data, during a task that requires subjects to choose simple manual actions. The race model is in turn informed by neurophysiological and behavioural decision paradigms, which offer a parsimonious mechanism for response selection with or without response biases that result from reward or memory influences. The race model reveals a clear distinction between lateral prefrontal and the pre-SMA, premotor cortex and parietal cortex. Activation of the latter regions correlates with the predictions of the race model for selection among competitive response schemas. In contrast, activation of the lateral prefrontal cortex correlates with switching to alternative successive responses, and other forms of non-random behaviour, dependent on the monitoring of responses in working memory. The analysis of patients at different stages of Parkinson’s disease, and healthy subjects with genetic polymorphisms affecting cortical dopamine metabolism, suggests an important role of dopamine in the selection of voluntary action. Behavioural consequences are seen not in simple performance parameters but rather in the degree of independence over successive choices. In addition to the differences in regional cortical activation, dynamic causal modelling of cortical networks reveals how Parkinson’s disease affects the interactions within an extended motor system. In a dopamine depleted off”-state, the selection of action becomes dependent on changes in prefrontal-premotor interactions rather than the normal dependence on changing prefrontal-preSMA interactions. The effect of Parkinson’s disease is qualitatively different from healthy aging of the motor system. We discuss the implications for understanding and improving behavioural control in health and neurological disease.

Biosketch: James Rowe is a behavioural neurologist, working at the Cambridge University Department of Clinical Neurosciences and the MRC Cognition and Brain Sciences Unit. He has recently been awarded a Wellcome Trust Senior Fellowship in Clinical Research to continue his work investigating behavioural and cognitive control in health and neurodegenerative disease. As a medical student at Downing College Cambridge reading Experimental Psychology (1991), he was inspired by the rapidly advancing research into cognitive, anatomic and pharmacological basis of neuropsychiatric disorders. He completed clinical medicine at Magdalen College Oxford (1994) and then with the support of a Wellcome Trust Clinical Training Fellowship he undertook his PhD at the Functional Imaging Laboratory of the Wellcome Department of Cognitive Neurology under the joint supervision of Prof. Richard Frackowiak and Prof. Dick Passingham (1998-2001). He returned to full time specialist training before resuming research in Cambridge as a consultant neurologist with a Wellcome Trust Intermediate Clinical Fellowship (2005-2009) to characterise the selection of rules and actions in the context of structural and neurodegenerative disease. His work emphasises the advantages of neuroimaging and in particular the additional insights into the mechanisms of disease and treatments that are available from the analysis of network connectivity. Over the next five years with collaborators from Cambridge Neuroscience he will combine computational modelling, psychopharmacology and neuroimaging to investigate new ways to enhance cognitive control in Parkinson’s disease and frontotemporal dementia.

This talk is part of the Clinical Neuroscience and Mental Health Symposium series.

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