A parametric fMRI investigation of context effects in sensorimotor timing and coordination

Center for Complex Systems and Brain Sciences, Florida Atlantic University, Boca Raton, FL 33431, USA.
Neuropsychologia (Impact Factor: 3.3). 04/2007; 45(4):673-84. DOI: 10.1016/j.neuropsychologia.2006.07.020
Source: PubMed


Mounting evidence suggests that information derived from environmental and behavioral sources is represented and maintained in the brain in a context-dependent manner. Here we investigate whether activity patterns underlying movements paced according to an internal temporal representation depend on how that representation is acquired during a previous pacing phase. We further investigate the degree to which context dependence is modulated by different time delays between pacing and continuation. BOLD activity was recorded while subjects moved at a rate established during a pacing interval involving either synchronized or syncopated coordination. Either no-delay or a 3, 6 or 9s delay was introduced prior to continuation. Context-dependent regions were identified when differences in neural activity generated during pacing continued to be observed during continuation despite the intervening delay. This pattern was observed in pre-SMA, bilateral lateral premotor cortex, bilateral declive and left inferior semi lunar lobule. These regions were more active when continuation followed from syncopation than from synchronization regardless of the delay length putatively revealing a context-dependent neural representation of the temporal interval. Alternatively, task related regions in which coordination-dependent differences did not persist following the delay, included bilateral putamen and supplementary-motor-area. This network may support the differential timing demands of coordination. A classic prefrontal-parietal-temporal working memory network was active only during continuation possibly providing mnemonic support for actively maintaining temporal information during the variable delay. This work provides support for the hypothesis that some timing information is represented in a task-dependent manner across broad cortical and subcortical networks.

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Available from: Olivier Oullier
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    • "Using the continuation paradigm, several studies have investigated both synchronization and syncopation to assess pacing7, 8). To study syncopation, the subjects were asked to make their taps coincide with the midpoint of each stimulus in the external pacing sequence. "
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    ABSTRACT: [Purpose] The purpose of this study was to investigate the influence of external pacing with periodic auditory stimuli on the control of periodic movement. [Subjects and Methods] Eighteen healthy subjects performed self-paced, synchronization-continuation, and syncopation-continuation tapping. Inter-onset intervals were 1,000, 2,000 and 5,000 ms. The variability of inter-tap intervals was compared between the different pacing conditions and between self-paced tapping and each continuation phase. [Results] There were no significant differences in the mean and standard deviation of the inter-tap interval between pacing conditions. For the 1,000 and 5,000 ms tasks, there were significant differences in the mean inter-tap interval following auditory pacing compared with self-pacing. For the 2,000 ms syncopation condition and 5,000 ms task, there were significant differences from self-pacing in the standard deviation of the inter-tap interval following auditory pacing. [Conclusion] These results suggest that the accuracy of periodic movement with intervals of 1,000 and 5,000 ms can be improved by the use of auditory pacing. However, the consistency of periodic movement is mainly dependent on the inherent skill of the individual; thus, improvement of consistency based on pacing is unlikely.
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    • "These effects could not be simply explained by sympathetic effects on vasoactivity, because these affect the whole brain vasculature but not particular structures. The analysis, however, has only yielded associations with specific parts of the entire network involved in motor preparation, performance and motor timing: [27], [36], [37] left SMA, left primary motor cortex left and right lentiform nuclei (which comprises the putamina and the globi pallidi) and the right cerebellar declive. Other regions like the middle occipital gyri or the superior parietal regions remained unaffected. "
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    ABSTRACT: It has been repeatedly shown that functional magnetic resonance imaging (fMRI) triggers distress and neuroendocrine response systems. Prior studies have revealed that sympathetic arousal increases, particularly at the beginning of the examination. Against this background it appears likely that those stress reactions during the scanning procedure may influence task performance and neural correlates. However, the question how sympathetic arousal elicited by the scanning procedure itself may act as a potential confounder of fMRI data remains unresolved today. Thirty-seven scanner naive healthy subjects performed a simple cued target detection task. Levels of salivary alpha amylase (sAA), as a biomarker for sympathetic activity, were assessed in samples obtained at several time points during the lab visit. SAA increased two times, immediately prior to scanning and at the end of the scanning procedure. Neural activation related to motor preparation and timing as well as task performance was positively correlated with the first increase. Furthermore, the first sAA increase was associated with task induced deactivation (TID) in frontal and parietal regions. However, these effects were restricted to the first part of the experiment. Consequently, this bias of scanner related sympathetic activation should be considered in future fMRI investigations. It is of particular importance for pharmacological investigations studying adrenergic agents and the comparison of groups with different stress vulnerabilities like patients and controls or adolescents and adults.
    Full-text · Article · Aug 2013 · PLoS ONE
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    • "Regarding neural mechanisms of different timing functions in healthy individuals, sensorimotor synchronisation of sub-second intervals is associated with activation of the dorsolateral prefrontal cortex (DLPFC) (Jantzen, Oullier, Marshall, Steinberg, & Kelso, 2007; Lewis, Wing, Pope, Praamstra, & Miall, 2004; Rubia et al., 1998; Rubia et al., 2000), the inferior frontal cortex (IFC) (Jantzen et al., 2007; Rao et al., 1997), medial frontal cortex (MFC) (Jantzen, Steinberg, & Kelso, 2004; Jantzen, Steinberg, & Jelso, 2005; Oullier, Jantzen, Steinberg, & Kelso, 2005), and the supplementary motor cortex (SMA) (Jantzen et al., 2004, 2005, 2007; Lewis et al., 2004; Rao et al., 1997; Riecker, Wildgruber, Mathiak, Grodd, & Ackermann, 2003; Rubia et al., 1998; Stoodley, Valera, & Schmahmann, 2012). The caudal SMA-proper sub-area appears to play a special role in sub-second synchronisation, as revealed by a meta-analytic contrast between functional neuroimaging studies of sensory vs. sensorimotor as well as sub-second vs. suprasecond timing tasks (Schwartze, Rothermich, & Kotz, 2012). "
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    ABSTRACT: Relatively recently, neurocognitive and neuroimaging studies have indicated that individuals with attention-deficit/hyperactivity disorder (ADHD) may have deficits in a range of timing functions and their underlying neural networks. Despite this evidence, timing deficits in ADHD are still somewhat neglected in the literature and mostly omitted from reviews on ADHD. There is therefore a lack of integrative reviews on the up-to-date evidence on neurocognitive and neurofunctional deficits of timing in ADHD and their significance with respect to other behavioural and cognitive deficits. The present review provides a synthetic overview of the evidence for neurocognitive and neurofunctional deficits in ADHD in timing functions, and integrates this evidence with the cognitive neuroscience literature of the neural substrates of timing. The review demonstrates that ADHD patients are consistently impaired in three major timing domains, in motor timing, perceptual timing and temporal foresight, comprising several timeframes spanning milliseconds, seconds, minutes and longer intervals up to years. The most consistent impairments in ADHD are found in sensorimotor synchronisation, duration discrimination, reproduction and delay discounting. These neurocognitive findings of timing deficits in ADHD are furthermore supported by functional neuroimaging studies that show dysfunctions in the key inferior fronto-striato-cerebellar and fronto-parietal networks that mediate the timing functions. Although there is evidence that these timing functions are inter-correlated with other executive functions that are well established to be impaired in the disorder, in particular working memory, attention, and to a lesser degree inhibitory control, the key timing deficits appear to survive when these functions are controlled for, suggesting independent cognitive deficits in the temporal domain. There is furthermore strong evidence for an association between timing deficits and behavioural measures of impulsiveness and inattention, suggesting that timing problems are key to the clinical behavioural profile of ADHD. Emerging evidence shows that the most common treatment of ADHD with the dopamine agonist and psychostimulant Methylphenidate attenuates most timing deficits in ADHD and normalises the abnormally blunted recruitment of the underlying fronto-striato-cerebellar networks. Timing function deficits in ADHD, therefore, next to executive function deficits, form an independent impairment domain, and should receive more attention in neuropsychological, neuroimaging, and pharmacological basic research as well as in translational research aimed to develop pharmacological or non-pharmacological treatment of abnormal timing behaviour and cognition in ADHD.
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