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Brain Activation in Motor Sequence Learning Is Related to the Level of Native Cortical Excitability  [PDF]
Silke Lissek, Guido S. Vallana, Onur Güntürkün, Hubert Dinse, Martin Tegenthoff
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0061863
Abstract: Cortical excitability may be subject to changes through training and learning. Motor training can increase cortical excitability in motor cortex, and facilitation of motor cortical excitability has been shown to be positively correlated with improvements in performance in simple motor tasks. Thus cortical excitability may tentatively be considered as a marker of learning and use-dependent plasticity. Previous studies focused on changes in cortical excitability brought about by learning processes, however, the relation between native levels of cortical excitability on the one hand and brain activation and behavioral parameters on the other is as yet unknown. In the present study we investigated the role of differential native motor cortical excitability for learning a motor sequencing task with regard to post-training changes in excitability, behavioral performance and involvement of brain regions. Our motor task required our participants to reproduce and improvise over a pre-learned motor sequence. Over both task conditions, participants with low cortical excitability (CElo) showed significantly higher BOLD activation in task-relevant brain regions than participants with high cortical excitability (CEhi). In contrast, CElo and CEhi groups did not exhibit differences in percentage of correct responses and improvisation level. Moreover, cortical excitability did not change significantly after learning and training in either group, with the exception of a significant decrease in facilitatory excitability in the CEhi group. The present data suggest that the native, unmanipulated level of cortical excitability is related to brain activation intensity, but not to performance quality. The higher BOLD mean signal intensity during the motor task might reflect a compensatory mechanism in CElo participants.
Dissociation of Motor Task-Induced Cortical Excitability and Pain Perception Changes in Healthy Volunteers  [PDF]
Magdalena S. Volz, Mariana Mendonca, Fernando S. Pinheiro, Huashun Cui, Marcus Santana, Felipe Fregni
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0034273
Abstract: Background There is evidence that interventions aiming at modulation of the motor cortex activity lead to pain reduction. In order to understand further the role of the motor cortex on pain modulation, we aimed to compare the behavioral (pressure pain threshold) and neurophysiological effects (transcranial magnetic stimulation (TMS) induced cortical excitability) across three different motor tasks. Methodology/Principal Findings Fifteen healthy male subjects were enrolled in this randomized, controlled, blinded, cross-over designed study. Three different tasks were tested including motor learning with and without visual feedback, and simple hand movements. Cortical excitability was assessed using single and paired-pulse TMS measures such as resting motor threshold (RMT), motor-evoked potential (MEP), intracortical facilitation (ICF), short intracortical inhibition (SICI), and cortical silent period (CSP). All tasks showed significant reduction in pain perception represented by an increase in pressure pain threshold compared to the control condition (untrained hand). ANOVA indicated a difference among the three tasks regarding motor cortex excitability change. There was a significant increase in motor cortex excitability (as indexed by MEP increase and CSP shortening) for the simple hand movements. Conclusions/Significance Although different motor tasks involving motor learning with and without visual feedback and simple hand movements appear to change pain perception similarly, it is likely that the neural mechanisms might not be the same as evidenced by differential effects in motor cortex excitability induced by these tasks. In addition, TMS-indexed motor excitability measures are not likely good markers to index the effects of motor-based tasks on pain perception in healthy subjects as other neural networks besides primary motor cortex might be involved with pain modulation during motor training.
Primary Sensory and Motor Cortex Excitability Are Co-Modulated in Response to Peripheral Electrical Nerve Stimulation  [PDF]
Siobhan M. Schabrun, Michael C. Ridding, Mary P. Galea, Paul W. Hodges, Lucinda S. Chipchase
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051298
Abstract: Peripheral electrical stimulation (PES) is a common clinical technique known to induce changes in corticomotor excitability; PES applied to induce a tetanic motor contraction increases, and PES at sub-motor threshold (sensory) intensities decreases, corticomotor excitability. Understanding of the mechanisms underlying these opposite changes in corticomotor excitability remains elusive. Modulation of primary sensory cortex (S1) excitability could underlie altered corticomotor excitability with PES. Here we examined whether changes in primary sensory (S1) and motor (M1) cortex excitability follow the same time-course when PES is applied using identical stimulus parameters. Corticomotor excitability was measured using transcranial magnetic stimulation (TMS) and sensory cortex excitability using somatosensory evoked potentials (SEPs) before and after 30 min of PES to right abductor pollicis brevis (APB). Two PES paradigms were tested in separate sessions; PES sufficient to induce a tetanic motor contraction (30–50 Hz; strong motor intensity) and PES at sub motor-threshold intensity (100 Hz). PES applied to induce strong activation of APB increased the size of the N20-P25 component, thought to reflect sensory processing at cortical level, and increased corticomotor excitability. PES at sensory intensity decreased the size of the P25-N33 component and reduced corticomotor excitability. A positive correlation was observed between the changes in amplitude of the cortical SEP components and corticomotor excitability following sensory and motor PES. Sensory PES also increased the sub-cortical P14-N20 SEP component. These findings provide evidence that PES results in co-modulation of S1 and M1 excitability, possibly due to cortico-cortical projections between S1 and M1. This mechanism may underpin changes in corticomotor excitability in response to afferent input generated by PES.
Electrophysiological Analysis of Cortical Excitability and Inhibition Using Transcranial Magnetic Stimulation for Understanding Aggressive Behaviors in Antisocial Personality Disorder  [PDF]
Zülküf PERDEC?,Kamil Nahit ?ZMENLER,Erhan Ali DO?RUER,Fatih ?ZDA?
N?ropsikiyatri Ar?ivi , 2009,
Abstract: Objective: Some biological researches on aggressive behaviors suggest that cortical excitability and inhibition imbalance cause behavioral problems like reactive aggression, impulsivity and inability to behavioral control. The purpose of the study is to evaluate whether cortical excitability-inhibition imbalance is responsible for aggressive behaviors in adult young men with antisocial personality disorder in which aggressive behavior is one of the key features. Method: We studied 42 subjects with antisocial personality disorder and 44 healthy controls matched for age and education level. The electrophysiology of cortical inhibition and excitability was measured with transcranial magnetic stimulation. SCID-I, SCID-II, Aggression Questionnaire, and Edinburg Handedness Inventory were performed to all subjects. Results: Motor threshold, cortical latency, and central motor conduction time, which are related with cortical excitability, have been found statistically significant lower on antisocial personality disorder group compared with healthy controls. There was no difference between two groups on cortical silent period which reflects cortical inhibitory mechanisms. Conclusion: The results indicate an increase in cortical motor excitability on antisocial personality disorder, and we suggest that the cortical imbalance might render the person prone to behavior problems. (Archives of Neuropsychiatry 2009; 46: 44-8)
Loss of Prestin Does Not Alter the Development of Auditory Cortical Dendritic Spines  [PDF]
L. J. Bogart,A. D. Levy,M. Gladstone,P. D. Allen,M. Zettel,J. R. Ison,A. E. Luebke,A. K. Majewska
Neural Plasticity , 2011, DOI: 10.1155/2011/305621
Abstract: Disturbance of sensory input during development can have disastrous effects on the development of sensory cortical areas. To examine how moderate perturbations of hearing can impact the development of primary auditory cortex, we examined markers of excitatory synapses in mice who lacked prestin, a protein responsible for somatic electromotility of cochlear outer hair cells. While auditory brain stem responses of these mice show an approximately 40?dB increase in threshold, we found that loss of prestin produced no changes in spine density or morphological characteristics on apical dendrites of cortical layer 5 pyramidal neurons. PSD-95 immunostaining also showed no changes in overall excitatory synapse density. Surprisingly, behavioral assessments of auditory function using the acoustic startle response showed only modest changes in prestin KO animals. These results suggest that moderate developmental hearing deficits produce minor changes in the excitatory connectivity of layer 5 neurons of primary auditory cortex and surprisingly mild auditory behavioral deficits in the startle response. 1. Introduction Early loss of sensory input can have profound effects on the development of sensory cortical areas. Early loss of vision has been shown to affect the development of both inhibitory and excitatory neurons in the visual cortex [1], and trimming of whiskers has similar effects on neurons in somatosensory barrel cortex [2]. While less extensively studied, developmental hearing loss has been shown to induce numerous changes in the response properties of auditory cortical neurons [3]. Sensorineural hearing loss in early postnatal life results in enhanced excitability and weakened inhibition in auditory cortex [4, 5]. Interestingly, even conductive hearing loss, which is a relatively mild deprivation of auditory experience, has similar effects on cortical auditory neurons [6]. In visual and somatosensory cortex, excitatory synapses have been shown to be sensitive to sensory manipulation. Manipulations of activity result in changes in the structure and dynamics of dendritic spines [7–11]. These structures are the postsynaptic sites of excitatory connections in the nervous system [12], making them likely substrates for structural plasticity. The shape of dendritic spines has long been thought to have important functional implications [13], and recent experiments have shown that the unique morphology of spines may allow them to compartmentalize calcium and implement synapse-specific plasticity. Thus the detailed morphology of dendritic spines is likely to be
Long-term sensory stimulation therapy improves hand function and restores cortical responsiveness in patients with chronic cerebral lesions. Three single case studies  [PDF]
Jan-Christoph Kattenstroth,Tobias Kalisch,Hubert R. Dinse
Frontiers in Human Neuroscience , 2012, DOI: 10.3389/fnhum.2012.00244
Abstract: Rehabilitation of sensorimotor impairment resulting from cerebral lesion (CL) utilizes task specific training and massed practice to drive reorganization and sensorimotor improvement due to induction of neuroplasticity mechanisms. Loss of sensory abilities often complicates recovery, and thus the individual's ability to use the affected body part for functional tasks. Therefore, the development of additional and alternative approaches that supplement, enhance, or even replace conventional training procedures would be advantageous. Repetitive sensory stimulation protocols (rSS) have been shown to evoke sensorimotor improvements of the affected limb in patients with chronic stroke. However, the possible impact of long-term rSS on sensorimotor performance of patients with CL, where the incident dated back many years remains unclear. The particular advantage of rSS is its passive nature, which does not require active participation of the subjects. Therefore, rSS can be applied in parallel to other occupations, making the intervention easier to implement and more acceptable to the individual. Here we report the effects of applying rSS for 8, 36, and 76 weeks to the paretic hand of three long-term patients with different types of CL. Different behavioral tests were used to assess sensory and/or sensorimotor performance of the upper extremities prior, after, and during the intervention. In one patient, the impact of long-term rSS on restoration of cortical activation was investigated by recording somatosensory evoked potentials (SEP). After long-term rSS all three patients showed considerable improvements of their sensory and motor abilities. In addition, almost normal evoked potentials could be recorded after rSS in one patient. Our data show that long-term rSS applied to patients with chronic CL can improve tactile and sensorimotor functions, which, however, developed in some cases only after many weeks of stimulation, and continued to further improve on a time scale of months.
Saccadic Performance and Cortical Excitability as Trait-Markers and State-Markers in Rapid Cycling Bipolar Disorder: A Two-Case Follow-Up Study  [PDF]
Jennifer Malsert,Nathalie Guyader,Alan Chauvin,Mircea Polosan,David Szekely,Christian Marendaz
Frontiers in Psychiatry , 2013, DOI: 10.3389/fpsyt.2012.00112
Abstract: Background: The understanding of physiopathology and cognitive impairments in mood disorders requires finding objective markers. Mood disorders have often been linked to hypometabolism in the prefrontal dorsolateral cortex, and to GABAergic and glutamatergic neurotransmission dysfunction. The present study aimed to discover whether saccadic tasks (involving DPLFC activity), and cortical excitability (involving GABA/Glutamate neurotransmission) could provide neuropsychophysical markers for mood disorders, and/or of its phases, in patients with rapid cycling bipolar disorders (rcBD). Methods: Two rcBD patients were followed for a cycle, and were compared to nine healthy controls. A saccade task, mixing prosaccades, antisaccades, and nosaccades, and an evaluation of cortical excitability using transcranial magnetic stimulation were performed. Results: We observed a deficit in antisaccade in patients independently of thymic phase, and in nosaccade in the manic phase only. Cortical excitability data revealed global intracortical deficits in all phases, switching according to cerebral hemisphere and thymic phase. Conclusion: Specific patterns of performance in saccade tasks and cortical excitability could characterize mood disorders (trait-markers) and its phases (state-markers). Moreover, a functional relationship between oculometric performance and cortical excitability is discussed.
Cortical Modulations Increase in Early Sessions with Brain-Machine Interface  [PDF]
Miriam Zacksenhouse, Mikhail A. Lebedev, Jose M. Carmena, Joseph E. O'Doherty, Craig Henriquez, Miguel A.L. Nicolelis
PLOS ONE , 2007, DOI: 10.1371/journal.pone.0000619
Abstract: Background During planning and execution of reaching movements, the activity of cortical motor neurons is modulated by a diversity of motor, sensory, and cognitive signals. Brain-machine interfaces (BMIs) extract part of these modulations to directly control artificial actuators. However, cortical modulations that emerge in the novel context of operating the BMI are poorly understood. Methodology/Principal Findings Here we analyzed the changes in neuronal modulations that occurred in different cortical motor areas as monkeys learned to use a BMI to control reaching movements. Using spike-train analysis methods we demonstrate that the modulations of the firing-rates of cortical neurons increased abruptly after the monkeys started operating the BMI. Regression analysis revealed that these enhanced modulations were not correlated with the kinematics of the movement. The initial enhancement in firing rate modulations declined gradually with subsequent training in parallel with the improvement in?behavioral performance. Conclusions/Significance We conclude that the enhanced modulations are related to computational tasks that are significant especially in novel motor contexts. Although the function and neuronal mechanism of the enhanced cortical modulations are open for further inquiries, we discuss their potential role in processing execution errors and representing corrective or explorative activity. These representations are expected to contribute to the formation of internal models of the external actuator and their decoding may facilitate BMI improvement.
Evolution of Premotor Cortical Excitability after Cathodal Inhibition of the Primary Motor Cortex: A Sham-Controlled Serial Navigated TMS Study  [PDF]
Sein Schmidt, Robert Fleischmann, Rouven Bathe-Peters, Kerstin Irlbacher, Stephan A. Brandt
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0057425
Abstract: Background Premotor cortical regions (PMC) play an important role in the orchestration of motor function, yet their role in compensatory mechanisms in a disturbed motor system is largely unclear. Previous studies are consistent in describing pronounced anatomical and functional connectivity between the PMC and the primary motor cortex (M1). Lesion studies consistently show compensatory adaptive changes in PMC neural activity following an M1 lesion. Non-invasive brain modification of PMC neural activity has shown compensatory neurophysiological aftereffects in M1. These studies have contributed to our understanding of how M1 responds to changes in PMC neural activity. Yet, the way in which the PMC responds to artificial inhibition of M1 neural activity is unclear. Here we investigate the neurophysiological consequences in the PMC and the behavioral consequences for motor performance of stimulation mediated M1 inhibition by cathodal transcranial direct current stimulation (tDCS). Purpose The primary goal was to determine how electrophysiological measures of PMC excitability change in order to compensate for inhibited M1 neural excitability and attenuated motor performance. Hypothesis Cathodal inhibition of M1 excitability leads to a compensatory increase of ipsilateral PMC excitability. Methods We enrolled 16 healthy participants in this randomized, double-blind, sham-controlled, crossover design study. All participants underwent navigated transcranial magnetic stimulation (nTMS) to identify PMC and M1 corticospinal projections as well as to evaluate electrophysiological measures of cortical, intracortical and interhemispheric excitability. Cortical M1 excitability was inhibited using cathodal tDCS. Finger-tapping speeds were used to examine motor function. Results Cathodal tDCS successfully reduced M1 excitability and motor performance speed. PMC excitability was increased for longer and was the only significant predictor of motor performance. Conclusion The PMC compensates for attenuated M1 excitability and contributes to motor performance maintenance.
TRESK channel contribution to nociceptive sensory neurons excitability: modulation by nerve injury
Astrid Tulleuda, Barbara Cokic, Gerard Callejo, Barbara Saiani, Jordi Serra, Xavier Gasull
Molecular Pain , 2011, DOI: 10.1186/1744-8069-7-30
Abstract: Here we describe that rat sciatic nerve axotomy induces hyperexcitability of L4-L5 DRG sensory neurons and decreases TRESK (K2P18.1) expression, a channel with a major contribution to total leak current in DRGs. While the expression of other channels from the same family did not significantly change, injury markers ATF3 and Cacna2d1 were highly upregulated. Similarly, acute sensory neuron dissociation (in vitro axotomy) produced marked hyperexcitability and similar total background currents compared with neurons injured in vivo. In addition, the sanshool derivative IBA, which blocked TRESK currents in transfected HEK293 cells and DRGs, increased intracellular calcium in 49% of DRG neurons in culture. Most IBA-responding neurons (71%) also responded to the TRPV1 agonist capsaicin, indicating that they were nociceptors. Additional evidence of a biological role of TRESK channels was provided by behavioral evidence of pain (flinching and licking), in vivo electrophysiological evidence of C-nociceptor activation following IBA injection in the rat hindpaw, and increased sensitivity to painful pressure after TRESK knockdown in vivo.In summary, our results clearly support an important role of TRESK channels in determining neuronal excitability in specific DRG neurons subpopulations, and show that axonal injury down-regulates TRESK channels, therefore contributing to neuronal hyperexcitability.After peripheral axon injury, nociceptors undergo a variety of changes resulting in persistent hyperexcitability and ectopic discharge, all potentially leading to altered pain perception, such as spontaneous pain, hyperalgesia and allodynia [1,2]. Constricting lesions and partial or total axotomy of peripheral nerves in animals produce behavioral alterations analogous to those seen in human neuropathic pain [3,4]. After injury to peripheral branches of nociceptors due to trauma, inflammation or other noxious stimuli, a variety of post-translational and transcriptional changes modifies
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