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Christian Beste - One of the best experts on this subject based on the ideXlab platform.

  • Effects of aging on sequential cognitive flexibility are associated with fronto-parietal processing deficits
    Brain Structure and Function, 2019
    Co-Authors: Franziska Giller, Christian Beste
    Abstract:

    Albeit cognitive flexibility is well known to decline in aging, it has not been considered that this ability often requires sequential task control. That is, one may re-use tasks that have previously been abandoned in favor of another task. It is unclear whether sequential cognitive flexibility is affected in aging and what Neurophysiological mechanisms and functional neuroanatomical structures are associated with these effects. We examined this question in a system Neurophysiological Study using EEG and source localization in healthy and elderly adults. We show that elderly people reveal deficient sequential cognitive flexibility. Elderly people encounter increased costs to overcome the inhibition of the lately abandoned task set that becomes relevant again and needs to be re-used. The Neurophysiological (EEG) data show that differences in sequential cognitive flexibility between young and elderly people emerge as a consequence of two independent, dysfunctional processes: (i) the ability to suppress task-irrelevant information and (ii) the ability to re-implement a previously abandoned task set during response selection. These independent processes were associated with activation differences in inferior frontal and inferior parietal regions. The Study reveals a new facet of cognitive flexibility dysfunctions in healthy elderlies.

  • specific properties of the si and sii somatosensory areas and their effects on motor control a system Neurophysiological Study
    Brain Structure & Function, 2018
    Co-Authors: Julia Friedrich, Moritz Muckschel, Christian Beste
    Abstract:

    Sensorimotor integration is essential for successful motor control and the somatosensory modality has been shown to have strong effects on the execution of motor plans. The primary (SI) and the secondary somatosensory (SII) cortices are known to differ in their neuroanatomical connections to prefrontal areas, as well as in their involvement to encode cognitive aspects of tactile processing. Here, we ask whether the area-specific processing architecture or the structural neuroanatomical connections with prefrontal areas determine the efficacy of sensorimotor integration processes for motor control. In a system Neurophysiological Study including EEG signal decomposition (i.e., residue iteration decomposition, RIDE) and source localization, we investigated this question using vibrotactile stimuli optimized for SI or SII processing. The behavioral data show that when being triggered via the SI area, inhibitory control of motor processes is stronger as when being triggered via the SII area. On a Neurophysiological level, these effects were reflected in the C-cluster as a result of a temporal decomposition of EEG data, indicating that the sensory processes affecting motor inhibition modulate the response selection level. These modulations were associated with a stronger activation of the right inferior frontal gyrus extending to the right middle frontal gyrus as parts of a network known to be involved in inhibitory motor control when response inhibition is triggered over SI. In addition, areas important for sensorimotor integration like the postcentral gyrus and superior parietal cortex showed activation differences. The data suggest that connection patterns are more important for sensorimotor integration and control than the more restricted area-specific processing architecture.

  • effects of high dose ethanol intoxication and hangover on cognitive flexibility
    Addiction Biology, 2018
    Co-Authors: Nicole Wolff, Philipp Gussek, Annkathrin Stock, Christian Beste
    Abstract:

    The effects of high-dose ethanol intoxication on cognitive flexibility processes are not well understood, and processes related to hangover after intoxication have remained even more elusive. Similarly, it is unknown in how far the complexity of cognitive flexibility processes is affected by intoxication and hangover effects. We performed a Neurophysiological Study applying high density electroencephalography (EEG) recording to analyze event-related potentials (ERPs) and perform source localization in a task switching paradigm which varied the complexity of task switching by means of memory demands. The results show that high-dose ethanol intoxication only affects task switching (i.e. cognitive flexibility processes) when memory processes are required to control task switching mechanisms, suggesting that even high doses of ethanol compromise cognitive processes when they are highly demanding. The EEG and source localization data show that these effects unfold by modulating response selection processes in the anterior cingulate cortex. Perceptual and attentional selection processes as well as working memory processes were only unspecifically modulated. In all subprocesses examined, there were no differences between the sober and hangover states, thus suggesting a fast recovery of cognitive flexibility after high-dose ethanol intoxication. We assume that the gamma-aminobutyric acid (GABAergic) system accounts for the observed effects, while they can hardly be explained by the dopaminergic system.

  • testing interactive effects of automatic and conflict control processes during response inhibition a system Neurophysiological Study
    NeuroImage, 2017
    Co-Authors: Witold X Chmielewski, Christian Beste
    Abstract:

    In everyday life successful acting often requires to inhibit automatic responses that might not be appropriate in the current situation. These response inhibition processes have been shown to become aggravated with increasing automaticity of pre-potent response tendencies. Likewise, it has been shown that inhibitory processes are complicated by a concurrent engagement in additional cognitive control processes (e.g. conflicting monitoring). Therefore, opposing processes (i.e. automaticity and cognitive control) seem to strongly impact response inhibition. However, possible interactive effects of automaticity and cognitive control for the modulation of response inhibition processes have yet not been examined. In the current Study we examine this question using a novel experimental paradigm combining a Go/NoGo with a Simon task in a system Neurophysiological approach combining EEG recordings with source localization analyses. The results show that response inhibition is less accurate in non-conflicting than in conflicting stimulus-response mappings. Thus it seems that conflicts and the resulting engagement in conflict monitoring processes, as reflected in the N2 amplitude, may foster response inhibition processes. This engagement in conflict monitoring processes leads to an increase in cognitive control, as reflected by an increased activity in the anterior and posterior cingulate areas, while simultaneously the automaticity of response tendencies is decreased. Most importantly, this Study suggests that the quality of conflict processes in anterior cingulate areas and especially the resulting interaction of cognitive control and automaticity of pre-potent response tendencies are important factors to consider, when it comes to the modulation of response inhibition processes.

  • perceptual conflict during sensorimotor integration processes a Neurophysiological Study in response inhibition
    Scientific Reports, 2016
    Co-Authors: Witold X Chmielewski, Christian Beste
    Abstract:

    A multitude of sensory inputs needs to be processed during sensorimotor integration. A crucial factor for detecting relevant information is its complexity, since information content can be conflicting at a perceptual level. This may be central to executive control processes, such as response inhibition. This EEG Study aims to investigate the system Neurophysiological mechanisms behind effects of perceptual conflict on response inhibition. We systematically modulated perceptual conflict by integrating a Global-local task with a Go/Nogo paradigm. The results show that conflicting perceptual information, in comparison to non-conflicting perceptual information, impairs response inhibition performance. This effect was evident regardless of whether the relevant information for response inhibition is displayed on the global, or local perceptual level. The Neurophysiological data suggests that early perceptual/ attentional processing stages do not underlie these modulations. Rather, processes at the response selection level (P3), play a role in changed response inhibition performance. This conflict-related impairment of inhibitory processes is associated with activation differences in (inferior) parietal areas (BA7 and BA40) and not as commonly found in the medial prefrontal areas. This suggests that various functional neuroanatomical structures may mediate response inhibition and that the functional neuroanatomical structures involved depend on the complexity of sensory integration processes.

P M Rossini - One of the best experts on this subject based on the ideXlab platform.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study.
    Journal of the neurological sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study
    Journal of the Neurological Sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    Abstract Objective : The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Subjects and method : Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. Results : In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Conclusions : Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

F Pauri - One of the best experts on this subject based on the ideXlab platform.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study.
    Journal of the neurological sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study
    Journal of the Neurological Sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    Abstract Objective : The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Subjects and method : Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. Results : In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Conclusions : Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

L Boffa - One of the best experts on this subject based on the ideXlab platform.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study.
    Journal of the neurological sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study
    Journal of the Neurological Sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    Abstract Objective : The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Subjects and method : Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. Results : In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Conclusions : Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

E Cassetta - One of the best experts on this subject based on the ideXlab platform.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study.
    Journal of the neurological sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.

  • Botulinum toxin type-A treatment in spastic paraparesis: a Neurophysiological Study
    Journal of the Neurological Sciences, 2000
    Co-Authors: F Pauri, L Boffa, E Cassetta, P Pasqualetti, P M Rossini
    Abstract:

    Abstract Objective : The aim of this Study was to verify the action of Botulinum toxin type-A (BoNT-A) by means of Neurophysiological techniques, in patients presenting lower limb spasticity and requiring BoNT-A injections in the calf muscles, due to the poor response to medical antispastic treatment. Subjects and method : Patients presenting paraparesis were enrolled. They underwent clinical evaluation for spasticity according to the Ashworth scale and Neurophysiological recordings including: motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) of the leg area; compound motor action potential (cMAP) to tibial nerve stimulation, F-wave, and H-reflex before the treatment and 24 h, 2 weeks and 1 month after the injection of BoNT-A. In all patients, gastrocnemius was treated and in some cases soleus or tibialis posterior muscles were also injected. Results : In all patients, BoNT-A injections induced a clear clinical improvement as showed by the reduced spasticity values of the Ashworth scale. A significant increment of MEP latency and central conduction time (CCT) duration were observed 2 weeks after the treatment only in the injected muscles. Conclusions : Prolonged MEP latencies and CCT after BoNT-A injections is probably due to a central alteration in responsiveness of spinal motor neurons to descending impulses from the corticospinal tracts. Such changes represent objective parameters heralding clinical efficacy of treatment.