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A neural mass model for simulating modulation of cortical activity with transcranial direct current stimulation
Abstract
INTRODUCTION
Neural mass models (NMM) provide insights into neuromodulatory mechanisms underlying alterations of cortical activity, as recorded by electroencephalography (EEG) [1]. In the human primary motor cortex (M1), neuromodulation can be induced by non-invasive brain stimulation (NIBS) [2]. We aimed to capture the origin of NIBS-induced neuromodulation by a thalamocortical NMM.
METHODS
A. Neural mass model
The NMM for a single cortical source comprised of 4 neuronal subpopulations, excitatory pyramidal neurons (ePN), excitatory interneurons (eIN), slow inhibitory interneurons (siIN), and fast inhibitory interneurons (fiIN) [3]. The NMM for the cortical source was coupled with another representing the thalamus [4], which comprised of 2 neuronal subpopulations, an excitatory thalamocortical (eTCN) and an inhibitory reticular-thalamic (iRT). The details of the thalamic NMM, parameterized to generate the alpha rhythm, are presented by Sotero et al.[4].
B. EEG data fitting
Eyes-open resting state EEG was recorded from the central site Cz using the international 10-20 system of scalp sites with Starstim (Neuroelectrics, Spain) before and immediately after 15min of anodal tDCS (current density=0.526A/m2) at the same site (Fig. 1) [5]. For each EEG recording, the average experimental power spectrum was analyzed from 0.25Hz to 50Hz for 25 successive 4s epochs. Then the NMM was fitted in the spectral domain using the Levenberg-Marquardt method for parameter optimization under quasi-stationarity assumptions, to identify the key parameters that determine the change in EEG spectral response.
RESULTS
The synaptic impulse response function (sIRF) of the dendritic tree of ePN, that receives presynaptic inputs to produce postsynaptic membrane potential alterations, was primarily changed (Fig. 1).
REFERENCES
1. Moran RJ, et al. Neuroimage. 2007;37(3):706-720.
2. Stagg CJ, Nitsche MA. Neuroscientist. 2011;17(1):37-53.
3. Zavaglia M, et al. J Neurosci Methods. 2006;157(2):317-29.
4. Sotero RC, et al. Neural Comput. 2007;19(2):478-512.
5. Dutta A, et al. Proc. IEEE NER 2013.
... However, online cerebellar anodal tDCS also decreased the learning rate during 'proportional EMG control' when compared to M1 anodal and sham tDCS which may be due to a different electrode montage in that experiment, as compared to the study conducted by Galea et Delineating the effects of anodal transcranial direct current stimulation on myoelectric control based on slow cortical potentials Anirban al [4]. In order to further investigate the effects of M1 anodal tDCS on motor performance, we conducted simultaneous electroencephalography (EEG) during self-initiated myoelectric control [5]. Our prior analysis [5] was based on resting state EEG which showed an increase of fractional power in the Theta band (4-8Hz) and decrease around "individual alpha frequency" in the Alpha band (8-13Hz) as shown by an illustrative example in Figure 2. Modeling suggests two primary effects of anodal tDCS -faster time constants of the synaptic impulse response function of the dendritic tree of the excitatory pyramidal neurons and an enhanced cortico-thalamic connectivity [5]. ...
... In order to further investigate the effects of M1 anodal tDCS on motor performance, we conducted simultaneous electroencephalography (EEG) during self-initiated myoelectric control [5]. Our prior analysis [5] was based on resting state EEG which showed an increase of fractional power in the Theta band (4-8Hz) and decrease around "individual alpha frequency" in the Alpha band (8-13Hz) as shown by an illustrative example in Figure 2. Modeling suggests two primary effects of anodal tDCS -faster time constants of the synaptic impulse response function of the dendritic tree of the excitatory pyramidal neurons and an enhanced cortico-thalamic connectivity [5]. ...
... In order to further investigate the effects of M1 anodal tDCS on motor performance, we conducted simultaneous electroencephalography (EEG) during self-initiated myoelectric control [5]. Our prior analysis [5] was based on resting state EEG which showed an increase of fractional power in the Theta band (4-8Hz) and decrease around "individual alpha frequency" in the Alpha band (8-13Hz) as shown by an illustrative example in Figure 2. Modeling suggests two primary effects of anodal tDCS -faster time constants of the synaptic impulse response function of the dendritic tree of the excitatory pyramidal neurons and an enhanced cortico-thalamic connectivity [5]. ...
Active cortical participation in rehabilitation procedures may be facilitated by modulating neuromuscular electrical stimulation (NMES) with electromyogram (EMG) and electroencephalogram (EEG) derived biopotentials, that represent simultaneous volitional effort. Here, the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function, and connections is called neuroplasticity. Neuroplasticity is involved in post-stroke functional disturbances, but also in rehabilitation. Beneficial neuroplastic changes may be facilitated with an adjuvant treatment with non-invasive brain stimulation (NIBS). This paper presents the results from a motor cortex anodal tDCS-EEG/EMG study in healthy volunteers. We investigated slow cortical potentials (SCP) during self-initiated movements. In this preliminary study, we found that anodal tDCS increased baseline-normalized post-tDCS mean power in the Theta band (4-8Hz) of resting state EEG (60.71% vs. 8.36%; p<0.01), and decreased the slope of post-tDCS SCP from motor task-related EEG (-6.43 au/sec vs. -4.86au/sec; p=0.021) when compared to sham tDCS. These preliminary results are discussed based on an accumulator model for spontaneous neural activity which postulates that a decision threshold applied to auto-correlated noise—in this case the output of a leaky stochastic accumulator—can account for the specific shape of the SCP prior to movement. We postulate that the anodal tDCS facilitated change in the slope of SCP may be related to the reaction times during a cued movement task, since our prior work showed that anodal tDCS decreases the delay in initiation of muscle contraction and increases the delay in termination of muscle activity.
... Among the above mentioned sources of variability, one of the key considerations in using tDCS to improve motor performance after stroke is how the stimulation modulates cerebral cortex [9,10]. Polarity of the electrodes is proved to be especially critical in individuals with stroke due to the spread of functional reorganization in the poststroke brain [10]. ...
... Among the above mentioned sources of variability, one of the key considerations in using tDCS to improve motor performance after stroke is how the stimulation modulates cerebral cortex [9,10]. Polarity of the electrodes is proved to be especially critical in individuals with stroke due to the spread of functional reorganization in the poststroke brain [10]. Given the hypothesis that rebalancing interhemispheric interactions and/or restoring excitability in the ipsilesional hemisphere is thought to be bene cial for post-stroke motor recovery [11,12], present studies show three montages of tDCS position modes to regulating the excitability of cerebral cortex in poststroke patients: upregulating excitability of the ipsilateral hemisphere through posing the anode tDCS (atDCS) on it; down regulating excitability of the contralateral hemisphere through posing the cathode tDCS (ctDCS) on it; ...
... upregulating the ipsilateral cortex and downregulating the contralateral cortex at the same time [13][14][15]. Some studies have found that the excitability or suppression to the brain is not a "one size ts all" approach to recovery following stroke [1,10,15]. It may be related to stroke states like motor impairment level or stroke period (acute, sub-acute or chronic). ...
Objective: We aimed at exploring the modulation of tDCS on spontaneous cortical activity through the changing of EEG rhythms to different tDCS montages and the interaction between cortical responses and variability factors of stroke individuals.
Methods: 19 stroke subjects underwent 4 tDCS sessions with 3 different tDCS montages (anodal (atDCS), cathodal (ctDCS) and bilateral (bi-tDCS)) and sham stimulation in a single-blind, randomized, controlled crossover design. We acquired resting-state (eyes closing and opening alternately) EEG data before and after tDCS, and calculated the spectral power of each frequency band. Paired-samples T test was applied to examine the difference of spectral power between pre- and post-stimulation of each montage. Three-way repeated measures analysis of variance with lesion hemispheres, stimulation montages and locations were carried out to investigate tDCS effects of different lesion, montages, and channel locations, and the interaction. Further, the effects of tDCS over time were analyzed applying three-way repeated ANOVAs as well with post trials, lesion hemispheres and channel locations separately to each montage. Finally, linear and quadratic regression model were used separately to describe the association between clinical factors of stroke patients and change of spectral power.
Results: We found that induced effect of tDCS was limited to the alpha rhythm of opening-state. atDCS increased the alpha power especially alpha1 (8-10 Hz) in local and distant areas of mainly frontal and partial. bi-tDCS affected the alpha power as well, but in a smaller area which mainly focused on alpha2 (10-13 Hz). ctDCS and sham had no effect on alpha rhythm. No significant difference of alpha band was found over the observed time range after the stimulation over. Results further showed that the quadratic model can better characterize the relationship between clinical factors and the tDCS effects of alpha rhythm than linear model. The changing of alpha especially alpha2 in contralateral hemisphere induced by atDCS was related to time since stroke, and alpha2 in ipsilateral hemisphere induced by bi-tDCS to motor impairment level.
Conclusion: Our results provide electrophysiological evidence that different tDCS montages in stroke subjects modulate rhythmic cortical activity of alpha band in different ways, and the effects maintained for at least 30 minutes. The tDCS modulation effect was related to clinical factors, especially the time since stroke and the level of motor impairment. These findings are of great significance for the knowledge on modulation effect to stroke patients and for therapeutic application of motor recovery following stroke.
... In our prior work, we have suggested that anodal tDCS enhances activity and excitability of the excitatory pyramidal neuron at a population level in a non-specific manner, and that μ-rhythm desynchronization is generated [5]. The excitation versus inhibition effects of acute tDCS on the population kinetics can produce a whole spectrum of EEG signals within the oscillatory regime of a neural mass model [6]. ...
... Prior works show a strong coupling between LFP and regional vascular responses even in the absence of spikes (i.e., sub-threshold depolarization) [31]. Moreover, our prior work showed an increase of fractional power in the Theta band (4-8Hz) and decrease around Bindividual alpha frequency^in the Alpha band (8-13Hz) following anodal tDCS [5]. In this study, NIRS complemented the electrophysiological measures with measurements of the changes in (cortical) tissue oxy-(HbO2), and deoxy-(Hb) hemoglobin concentration roughly underlying Cz location. ...
... In our prior work, we have suggested that anodal tDCS enhances activity and excitability of the excitatory pyramidal neuron at a population level in a non-specific manner, and that µ-rhythm desynchronization is generated [5]. The excitation versus inhibition effects of acute tDCS on the population kinetics can produce a whole spectrum of EEG signals within the oscillatory regime of a neural mass model [6]. ...
... Prior works show a strong coupling between LFP and regional vascular responses even in the absence of spikes (i.e., sub-threshold depolarization) [31]. Moreover, our prior work showed an increase of fractional power in the Theta band (4-8Hz) and decrease around "individual alpha frequency" in the Alpha band (8-13Hz) following anodal tDCS [5]. In this study, NIRS complemented the electrophysiological measures with measurements of the changes in (cortical) tissue oxy-( 2 HbO ), and deoxy-( Hb ) hemoglobin concentration roughly underlying Cz location. ...
Objective: A method for electroencephalography (EEG) - near-infrared spectroscopy (NIRS) based assessment of neurovascular coupling (NVC) during anodal transcranial direct current stimulation (tDCS) is presented.
Methods: Anodal tDCS modulates cortical neural activity leading to a hemodynamic response, which was used to identify impaired NVC functionality. In this study, the hemodynamic response was estimated with NIRS. NIRS recorded changes in oxy-hemoglobin ( ) and deoxy-hemoglobin ( ) concentrations during anodal tDCS-induced activation of the cortical region located under the electrode and in-between the light sources and detectors. Anodal tDCS-induced alterations in the underlying neuronal current generators were also captured with EEG. Then, a method for the assessment of NVC underlying the site of anodal tDCS was proposed that leverages the Hilbert-Huang Transform.
Results: The case series including four chronic (>6 months) ischemic stroke survivors (3 males, 1 female from age 31 to 76) showed non-stationary effects of anodal tDCS on EEG that correlated with the response. Here, the initial dip in at the beginning of anodal tDCS corresponded with an increase in the log-transformed mean-power of EEG within 0.5Hz-11.25Hz frequency band. The cross-correlation coefficient changed signs but was comparable across subjects during and after anodal tDCS. The log-transformed mean-power of EEG lagged response during tDCS but then led post-tDCS.
Conclusion: This case series demonstrates changes in the degree of neurovascular coupling to a 0.526A/m2 square-pulse (0-30sec) of anodal tDCS. The initial dip in needs to be carefully investigated in a larger cohort, for example in patients with small vessel disease.
... In our prior work, we have suggested that anodal tDCS enhances activity and excitability of the excitatory pyramidal neuron at a population level in a non-specific manner, and that µ-rhythm desynchronization is generated [5]. The excitation versus inhibition effects of acute tDCS on the population kinetics can produce a whole spectrum of EEG signals within the oscillatory regime of a neural mass model [6]. ...
... Prior works show a strong coupling between LFP and regional vascular responses even in the absence of spikes (i.e., sub-threshold depolarization) [31]. Moreover, our prior work showed an increase of fractional power in the Theta band (4-8Hz) and decrease around "individual alpha frequency" in the Alpha band (8-13Hz) following anodal tDCS [5]. In this study, NIRS complemented the electrophysiological measures with measurements of the changes in (cortical) tissue oxy-( 2 HbO ), and deoxy-( Hb ) hemoglobin concentration roughly underlying Cz location. ...
A method for electroencephalography (EEG) - near-infrared spectroscopy (NIRS) based assessment of neurovascular coupling (NVC) during anodal transcranial direct current stimulation (tDCS). Anodal tDCS modulates cortical neural activity leading to a hemodynamic response, which was used to identify impaired NVC functionality. In this study, the hemodynamic response was estimated with NIRS. NIRS recorded changes in oxy-hemoglobin (HbO2) and deoxy-hemoglobin (Hb) concentrations during anodal tDCS-induced activation of the cortical region located under the electrode and in-between the light sources and detectors. Anodal tDCS-induced alterations in the underlying neuronal current generators were also captured with EEG. Then, a method for the assessment of NVC underlying the site of anodal tDCS was proposed that leverages the Hilbert-Huang Transform. The case series including four chronic (>6 months) ischemic stroke survivors (3 males, 1 female from age 31 to 76) showed non-stationary effects of anodal tDCS on EEG that correlated with the HbO2 response. Here, the initial dip in HbO2 at the beginning of anodal tDCS corresponded with an increase in the log-transformed mean-power of EEG within 0.5Hz-11.25Hz frequency band. The cross-correlation coefficient changed signs but was comparable across subjects during and after anodal tDCS. The log-transformed mean-power of EEG lagged HbO2 response during tDCS but then led post-tDCS. This case series demonstrated changes in the degree of neurovascular coupling to a 0.526 A/m(2) square-pulse (0-30 s) of anodal tDCS. The initial dip in HbO2 needs to be carefully investigated in a larger cohort, for example in patients with small vessel disease.
Transcranial direct current stimulation (tDCS) has been shown to modulate cortical neural activity (Nitsche and Paulus 2000). During neural activity, the electric currents from excitable membranes of brain tissue superimpose at a given location in the extracellular medium and generate a potential, which is referred to as the electroencephalogram (EEG) when recorded from the scalp (Nunez and Srinivasan 2006). Respective neural activity has been shown to be closely related, spatially and temporally, to cerebral blood flow (CBF) that supplies glucose via neurovascular coupling (Girouard and Iadecola 2006). The hemodynamic response to neural activity can be captured by near-infrared spectroscopy (NIRS), which enables continuous monitoring of cerebral oxygenation and blood volume (Siesler et al. 2008). Here, the CBF is increased in the brain regions with neural activity via metabolic coupling mechanisms (Attwell et al. 2010). Cerebral autoregulation mechanisms ensure that the blood
flow is maintained during changes in the perfusion pressure (Lucas et al. 2010). We proposed a phenomological model for metabolic coupling mechanisms (Attwell et al. 2010) to capture cerebrovascular reactivity (CVR) that represented the capacity of blood vessels to dilate during anodal tDCS due to neuronal activity-caused increased demands of oxygen (Dutta et al. 2013). Crosssectional studies suggest that impaired cerebral hemodynamics precedes stroke and transient ischaemic attacks (TIA). CVR reflects the capacity of blood vessels to dilate, and is an important marker for brain vascular reserve (Markus and Cullinane 2001). Therefore, cerebrovascular reserve capacity may have a predictive value for the risk of cerebral infarction in patients with reduced cerebrovascular reserve capacity such that it might evolve as a part of routine diagnostic neuroangiologic program (Stoll and Hamann 2002).
The paper presents a point of care testing device for neurovascular coupling (NVC) from simultaneous recording of electroencephalogram (EEG) and near infra red spectroscopy (NIRS) during anodal transcranial direct current stimulation (tDCS). Here, anodal tDCS modulated cortical neural activity leading to hemodynamic response can be used to identify impaired cerebral microvessels functionality. The impairments in the cerebral microvessels functionality may lead to impairments in the cerebrovascular reactivity (CVR) where severely reduced CVR predicts the chances of transient ischemic attack (TIA) and ipsilateral stroke. The neural and hemodynamic responses to anodal tDCS were studied through joint imaging with EEG and NIRS where NIRS provided optical measurement of changes in tissue oxy-( ) and deoxy-( ) haemoglobin concentration and EEG captured alterations in the underlying neuronal current generators. Then, a cross-correlation method for the assessment of neurovascular coupling (NVC) underlying the site of anodal tDCS is presented. The feasibility studies on healthy subjects and stroke survivors showed detectable changes in the EEG and NIRS responses to a 0.526A/m2 of anodal tDCS. The NIRS system was bench tested on 15 healthy subjects that showed a statistically significant (p<0.01) difference in the signal to noise ratio (SNR) between the on and off states of anodal tDCS where the mean SNR of the NIRS device was found to be 42.33±1.33dB in the on state and 40.67±1.23dB in the off state. Moreover, the clinical study conducted on 14 stroke survivors revealed that the lesioned hemisphere with impaired circulation showed significantly (p<0.01) less change in than the non-lesioned side in response to anodal tDCS. The EEG study on healthy subjects showed a statistically significant (p<0.05) decrease around "individual alpha frequency" in the Alpha band (8-13Hz) following anodal tDCS. Moreover, the joint EEG-NIRS imaging on 4 stroke survivors showed an immediate increase in the Theta band (4Hz-8Hz) EEG activity after the start of anodal tDCS at the non-lesioned hemisphere. Furthermore, cross-correlation function revealed a significant (95 percent confidence interval) negative cross-correlation only at the non-lesioned hemisphere during anodal tDCS where the log-transformed mean-power of EEG within 0.5Hz-11.25Hz lagged response in one of the stroke survivors with white matter lesions. Therefore, it was concluded that anodal tDCS can perturb local neural and vascular activity (via NVC) which can be used for assessing regional NVC functionality where confirmatory clinical studies are required.
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