Posts Tagged plasticity

[ARTICLE] Effects of 8-week sensory electrical stimulation combined with motor training on EEG-EMG coherence and motor function in individuals with stroke – Full Text

 

Abstract

The peripheral sensory system is critical to regulating motor plasticity and motor recovery. Peripheral electrical stimulation (ES) can generate constant and adequate sensory input to influence the excitability of the motor cortex. The aim of this proof of concept study was to assess whether ES prior to each hand function training session for eight weeks can better improve neuromuscular control and hand function in chronic stroke individuals and change electroencephalography-electromyography (EEG-EMG) coherence, as compared to the control (sham ES). We recruited twelve subjects and randomly assigned them into ES and control groups. Both groups received 20-minute hand function training twice a week, and the ES group received 40-minute ES on the median nerve of the affected side before each training session. The control group received sham ES. EEG, EMG and Fugl-Meyer Assessment (FMA) were collected at four different time points. The corticomuscular coherence (CMC) in the ES group at fourth weeks was significantly higher (p = 0.004) as compared to the control group. The notable increment of FMA at eight weeks and follow-up was found only in the ES group. The eight-week rehabilitation program that implemented peripheral ES sessions prior to function training has a potential to improve neuromuscular control and hand function in chronic stroke individuals.

Introduction

Stroke is one of the leading contributing factors to the loss of functional abilities and independence in daily life in adults1. The most common and widely observed impairment following stroke is motor impairment, which can be regarded as a loss or limitation of function in muscle control or movement2,3,4,5. Most stroke survivors later regain the ability to walk independently, but only fewer than 50% of them will have fully recovered upper extremity functions6,7. From a review focusing on motor recovery after stroke, it has been indicated that the recovery of both arm and hand function among subacute and chronic stroke survivors is limited in current neural rehabilitation settings4; therefore, additional management with activating plasticity before or during performing motor training is necessary for better motor recovery.

The fundamental principle of stroke rehabilitation is inducing brain plasticity by sensory or proprioceptive input in order to facilitate motor functions8,9. It has been demonstrated that strong sensory input can induce plastic changes in the motor cortex via direct or indirect pathways10,11,12,13,14,15,16,17. In this case, electrical stimulation (ES) that provides steady and adequate somatosensory input can be an ideal method of stimulating the motor cortex.

Recent studies using functional magnetic resonance imaging (fMRI) or transcranial magnetic stimulation (TMS) suggest that ES on peripheral nerves can increase motor-evoked potential (MEP)18,19,20, increase the active voxel count in the corresponding motor cortex13, and increase blood-oxygen-level dependent (BOLD) signals in fMRI, suggesting peripheral ES induced higher excitability and activation level of cortical neurons21. Since the expansion of the motor cortical area or increase in the excitability of neural circuits is associated with learning new motor skills22,23,24,25,26, clinicians should take advantage and assist patients with stroke on motor tasks training during this period of time. Celnik and colleagues27 found that the hand function of chronic stroke subjects improved immediately after two-hour peripheral nerve stimulation combined with functional training, and the effect lasted for one day. Based on previous studies, the ES that increases corticomuscular excitability may turn out to be an ideal intervention added prior to traditional motor training to “activate” the neural circuit, so that patients may get the most out of the training. According to a recent study that applied single session peripheral ES on post-stroke individuals, the corticomuscular coherence (CMC), which is the synchronization level between EEG and EMG, increased significantly and was accompanied by improvement in the steadiness of force output28.

To our knowledge, however, there is no study investigating the long-term effect of ES combined with functional training on both motor performance and cortical excitability. We targeted the median nerve because its distribution covered the dorsal side of index, middle, and half of ring finger and the palmar side of the first three fingers and half of the ring finger. Besides, median nerve is in charge of the flexion of the first three fingers, which combined they accounts for most of the functional tasks of hand. Therefore, the purpose of this pilot study was to preliminarily evaluate the effect of eight-week ES-combined hand functional training among chronic stroke patients based on CMC and motor performance. We followed up for four weeks after the intervention ceased and examined the lasting effect. We hypothesized that those who received intervention with ES would have better hand function and higher CMC than those who received intervention with sham ES. We also hypothesized that the effect would last for at least four weeks during our follow-up.[…]

Continue —> Effects of 8-week sensory electrical stimulation combined with motor training on EEG-EMG coherence and motor function in individuals with stroke | Scientific Reports

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[ARTICLE] Comparison of the Efficacy of a Real-Time and Offline Associative Brain-Computer-Interface – Full Text

An associative brain-computer-interface (BCI) that correlates in time a peripherally generated afferent volley with the peak negativity (PN) of the movement related cortical potential (MRCP) induces plastic changes in the human motor cortex. However, in this associative BCI the movement timed to a cue is not detected in real time. Thus, possible changes in reaction time caused by factors such as attention shifts or fatigue will lead to a decreased accuracy, less pairings, and likely reduced plasticity. The aim of the current study was to compare the effectiveness of this associative BCI intervention on plasticity induction when the MRCP PN time is pre-determined from a training data set (BCIoffline), or detected online (BCIonline). Ten healthy participants completed both interventions in randomized order. The average detection accuracy for the BCIonline intervention was 71 ± 3% with 2.8 ± 0.7 min-1 false detections. For the BCIonline intervention the PN did not differ significantly between the training set and the actual intervention (t9 = 0.87, p = 0.41). The peak-to-peak motor evoked potentials (MEPs) were quantified prior to, immediately following, and 30 min after the cessation of each intervention. MEP results revealed a significant main effect of time, F(2,18) = 4.46, p = 0.027. The mean TA MEP amplitudes were significantly larger 30 min after (277 ± 72 μV) the BCI interventions compared to pre-intervention MEPs (233 ± 64 μV) regardless of intervention type and stimulation intensity (p = 0.029). These results provide further strong support for the associative nature of the associative BCI but also suggest that they likely differ to the associative long-term potentiation protocol they were modeled on in the exact sites of plasticity.

Introduction

Since Daly et al. (2009) proposed the possibility of a Brain-Computer-Interface (BCI) designed for neuromodulation of stroke patients, the field has rapidly expanded with numerous novel BCIs being introduced and tested in the clinic (Ang et al., 2010Broetz et al., 2010Cincotti et al., 2012Li et al., 2013Ramos-Murguialday et al., 2013Mukaino et al., 2014Young et al., 2014Pichiorri et al., 2015Mrachacz-Kersting et al., 2016). To date the main focus has been on upper limb rehabilitation with relatively few targeting lower limb function (for a review see, Teo and Chew, 2014Cervera et al., 2018). In addition, only one group has investigated patients in the sub-acute phases of stroke (Mrachacz-Kersting et al., 2017b), presumably due to the relatively stable condition that a chronic stroke patient presents. Effects from the use of a BCI are thus easier to control since patients in the acute and subacute phase are prone to spontaneous biological recovery (Krakauer and Marshall, 2015).

Typically, BCIs function by collecting the brain signals during a specific state such as performing a movement or motor imagery, extracting features of interest and then translating these into commands for external device control (Daly and Wolpaw, 2008). The available non-invasive BCIs for stroke patients have implemented both electroencephalography (EEG) or near-infrared spectroscopy (NIRS) to acquire the brain signals, extracted various spectral and temporal features [e.g., sensorimotor rhythm, movement related cortical potentials (MR)] and provided diverse types of afferent feedback to the patient such as those generated from using robotic devices, virtual reality or by driving direct nerve or muscular electrical stimulation (for review see, Cervera et al., 2018).

A vital component of any BCI designed for rehabilitation of lost motor function in stroke patients, is that the physiological theories behind learning and memory must be satisfied. One of the most influential theories was proposed in 1949 by Hebb (2005) from which we know that “Cells that fire together, wire together.” Although Hebb proposed his theory on theoretical grounds, animal data later verified that if the pre-synaptic neuron is activated simultaneously with the post-synaptic cell, plasticity is induced, often referred to as long-term potentiation (for a review see, Cooke and Bliss, 2006). In 2000, a group from Rostock University were the first to demonstrate long-term potentiation like plasticity in the intact human brain (Stefan, 2000) with later applications to lower limb muscles (Mrachacz-Kersting et al., 2007). In this intervention [paired associative stimulation (PAS)], a peripheral nerve that innervates the target muscle is activated using a single electrical stimulus and once the generated afferent volley has arrived at the motor cortex, a single non-invasive transcranial magnetic stimulus (TMS) is provided to that area of the motor cortex that has a direct connection to the target muscle (for a review see, Suppa et al., 2017).

In a modified version of PAS, the TMS stimulus has been replaced by the movement related cortical potential (MRCP) (Mrachacz-Kersting et al., 2012). The MRCP, that can be readily measured using EEG, is a slow negative potential that arises approximately 1–2 s prior to movement execution or imagination and attains its peak negativity at the time of movement execution (Walter et al., 1964). This intervention, also termed an associative BCI, induces significant plasticity of the cortical projections to the target muscle and leads to significant functional improvements in chronic and subacute stroke patients (Mrachacz-Kersting et al., 20162017b). In the first phase, patients are asked to attempt 30–50 movements (dorsiflexion of the foot), timed to a visual cue and they receive no sensory feedback. The time of the peak negativity (PN) of the resulting MRCP for every trial is extracted and an average calculated. During the second phase (the actual associative BCI intervention), this time is used to trigger the electrical stimulation of the target nerve such that the generated afferent volley arrives at the motor cortex at precisely peak negativity. Typically, 30–50 such pairings are performed over 3–12 sessions. Since the trigger of the electrical stimulator is not based on the online detection of the MRCP during the second phase, this intervention does not represent a BCI in the classical sense. In the current study the aim was to compare the effects of this associative BCI intervention on plasticity induction as quantified by the motor evoked potential (MEP) following TMS when the MRCP PN time is determined from the phase one trials (BCIoffline modus) or detected during the second phase by using the phase one trials as a training data set (BCIonline modus).[…]

 

Continue —> Frontiers | Comparison of the Efficacy of a Real-Time and Offline Associative Brain-Computer-Interface | Neuroscience

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[WEB SITE] Researchers demonstrate synaptic plasticity in new-born neurons

Repeated stimulation enlarges dendritic spines

Even in adult brains, new neurons are generated throughout a lifetime. In a publication in the scientific journal PNAS, a research group led by Goethe University describes plastic changes of adult-born neurons in the hippocampus, a critical region for learning: frequent nerve signals enlarge the spines on neuronal dendrites, which in turn enables contact with the existing neural network.

Practice makes perfect, and constant repetition promotes the ability to remember. Researchers have been aware for some time that repeated electrical stimulation strengthens neuron connections (synapses) in the brain. It is similar to the way a frequently used trail gradually widens into a path. Conversely, if rarely used, synapses can also be removed – for example, when the vocabulary of a foreign language is forgotten after leaving school because it is no longer practiced. Researchers designate the ability to change interconnections permanently and as needed as the plasticity of the brain.

Plasticity is especially important in the hippocampus, a primary region associated with long-term memory, in which new neurons are formed throughout life. The research groups led by Dr Stephan Schwarzacher (Goethe University), Professor Peter Jedlicka (Goethe University and Justus Liebig University in Gieβen) and Dr Hermann Cuntz (FIAS, Frankfurt) therefore studied the long-term plasticity of synapses in new-born hippocampal granule cells. Synaptic interconnections between neurons are predominantly anchored on small thorny protrusions on the dendrites called spines. The dendrites of most neurons are covered with these spines, similar to the thorns on a rose stem.

In their recently published work, the scientists were able to demonstrate for the first time that synaptic plasticity in new-born neurons is connected to long-term structural changes in the dendritic spines: repeated electrical stimulation strengthens the synapses by enlarging their spines. A particularly surprising observation was that the overall size and number of spines did not change: when the stimulation strengthened a group of synapses, and their dendritic spines enlarged, a different group of synapses that were not being stimulated simultaneously became weaker and their dendritic spines shrank.

“This observation was only technically possible because our students Tassilo Jungenitz and Marcel Beining succeeded for the first time in examining plastic changes in stimulated and non-stimulated dendritic spines within individual new-born cells using 2-photon microscopy and viral labeling,” says Stephan Schwarzacher from the Institute for Anatomy at the University Hospital Frankfurt. Peter Jedlicka adds: “The enlargement of stimulated synapses and the shrinking of non-stimulated synapses was at equilibrium. Our computer models predict that this is important for maintaining neuron activity and ensuring their survival.”

The scientists now want to study the impenetrable, spiny forest of new-born neuron dendrites in detail. They hope to better understand how the equilibrated changes in dendritic spines and their synapses contribute the efficient storing of information and consequently to learning processes in the hippocampus.

 

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[ARTICLE] Shaping neuroplasticity by using powered exoskeletons in patients with stroke: a randomized clinical trial – Full Text

Abstract

Background

The use of neurorobotic devices may improve gait recovery by entraining specific brain plasticity mechanisms, which may be a key issue for successful rehabilitation using such approach. We assessed whether the wearable exoskeleton, Ekso™, could get higher gait performance than conventional overground gait training (OGT) in patients with hemiparesis due to stroke in a chronic phase, and foster the recovery of specific brain plasticity mechanisms.

Methods

We enrolled forty patients in a prospective, pre-post, randomized clinical study. Twenty patients underwent Ekso™ gait training (EGT) (45-min/session, five times/week), in addition to overground gait therapy, whilst 20 patients practiced an OGT of the same duration. All individuals were evaluated about gait performance (10 m walking test), gait cycle, muscle activation pattern (by recording surface electromyography from lower limb muscles), frontoparietal effective connectivity (FPEC) by using EEG, cortico-spinal excitability (CSE), and sensory-motor integration (SMI) from both primary motor areas by using Transcranial Magnetic Stimulation paradigm before and after the gait training.

Results

A significant effect size was found in the EGT-induced improvement in the 10 m walking test (d = 0.9, p < 0.001), CSE in the affected side (d = 0.7, p = 0.001), SMI in the affected side (d = 0.5, p = 0.03), overall gait quality (d = 0.8, p = 0.001), hip and knee muscle activation (d = 0.8, p = 0.001), and FPEC (d = 0.8, p = 0.001). The strengthening of FPEC (r = 0.601, p < 0.001), the increase of SMI in the affected side (r = 0.554, p < 0.001), and the decrease of SMI in the unaffected side (r = − 0.540, p < 0.001) were the most important factors correlated with the clinical improvement.

Conclusions

Ekso™ gait training seems promising in gait rehabilitation for post-stroke patients, besides OGT. Our study proposes a putative neurophysiological basis supporting Ekso™ after-effects. This knowledge may be useful to plan highly patient-tailored gait rehabilitation protocols.

Background

Most of the patients with stroke experience a restriction of their mobility. Gait impairment after stroke mainly depends on deficits in functional ambulation capacity, balance, walking velocity, cadence, stride length, and muscle activation pattern, resulting in a longer gait cycle duration and lower than normal stance/swing ratio in the affected side, paralleled by a shorter gait cycle duration and a higher than normal stance/swing ratio in the unaffected side [1].

Conventional gait training often offers non-completely satisfactory results. Specifically, patients with stroke receiving intensive gait training with or without body weight support (BWS) may not improve in walking ability more than those who are not receiving the same treatment (with the exception of walking speed and endurance) [2345]. Moreover, only patients with stroke who are able to walk benefit most from such an intervention [2345]. Therefore, there is growing effort to increase the efficacy of gait rehabilitation for stroke patients by using advanced technical devices. Neurorobotic devices, including robotic-assisted gait training (RAGT) with BWS, result in a more likely achievement of independent walking when coupled with overground gait training (OGT) in patients with stroke. Specifically, RAGT combined with OGT has an additional beneficial effect on functional ambulation outcomes, although depending on the duration and intensity of RAGT [67]. Further, RAGT requires a more active subject participation in gait training as compared to the traditional OGT, which is a vital feature of gait rehabilitation [78].

Even though no substantial differences have been reported among the different types of RAGT devices [9], a main problem with neurorobotic devices is the provision for the patient of a real-world setting ambulation [1011]. To this end, wearable powered exoskeletons, e.g., the Ekso™ (Ekso™ Bionics, Richmond, CA, USA), have been designed to improve OGT in neurologic patients.

Notwithstanding, the efficacy of wearable powered exoskeletons in improving functional ambulation capacity (including gait pattern, step length, walking speed and endurance, balance and coordination) has not been definitively proven, and any further benefit in terms of gait performance remains to be confirmed. However, a recent study showed that Ekso™ could improve functional ambulation capacity in patients with sub-acute and chronic stroke [12]. Therefore, a first aim of our study was to assess whether Ekso™ is useful in improving functional ambulation capacity and gait performance in chronic post-stroke patients compared to conventional OGT.

The neurophysiologic mechanisms harnessed by powered exoskeletons to favor the recovery of functional ambulation capacity are still unclear. It is argued that the efficacy of neurorobotics in improving functional ambulation capacity depends on the high frequency and intensity of repetition of task-oriented movements [13]. This could guarantee a potentially stronger entrainment of the neuroplasticity mechanisms related to motor learning and function recovery following brain injury, including sensorimotor plasticity, frontoparietal effective connectivity (FPEC), and transcallosal inhibition, as compared to conventional therapy [141516]. Moreover, the generation and strengthening of new connections supporting the learned behaviors, and the steady recruitment of these neural connections as preferential to the learned behaviors occur through these mechanisms, thus making the re-learned abilities long lasting [131417181920212223].

Such neurophysiologic mechanisms have been tested in neurorobotic rehabilitation using stationary exoskeletons (e.g. Lokomat™) [1314]. Therefore, the second aim of our study was to assess whether there are specific neurophysiological mechanisms (among those related to sensorimotor plasticity, FPEC, and transcallosal inhibition) by which Ekso™ improves functional ambulation capacity in the chronic post-stroke phase. The importance of knowing these mechanisms is remarkable in order to implement patient-tailored rehabilitative training, given that any further advance in motor function recovery mainly relies on motor rehabilitation training, whereas spontaneous motor recovery occurs within 6 months of a stroke [24]. This is also the reason why we focused our study on patients with chronic stroke.[…}

 

Continue —> Shaping neuroplasticity by using powered exoskeletons in patients with stroke: a randomized clinical trial | Journal of NeuroEngineering and Rehabilitation | Full Text

Fig. 2 Ekso™ device

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[ARTICLE] Cerebral Reorganization in Subacute Stroke Survivors after Virtual Reality-Based Training: A Preliminary Study – Full Text

Abstract

Background

Functional magnetic resonance imaging (fMRI) is a promising method for quantifying brain recovery and investigating the intervention-induced changes in corticomotor excitability after stroke. This study aimed to evaluate cortical reorganization subsequent to virtual reality-enhanced treadmill (VRET) training in subacute stroke survivors.

Methods

Eight participants with ischemic stroke underwent VRET for 5 sections per week and for 3 weeks. fMRI was conducted to quantify the activity of selected brain regions when the subject performed ankle dorsiflexion. Gait speed and clinical scales were also measured before and after intervention.

Results

Increased activation in the primary sensorimotor cortex of the lesioned hemisphere and supplementary motor areas of both sides for the paretic foot (p < 0.01) was observed postintervention. Statistically significant improvements were observed in gait velocity (p < 0.05). The change in voxel counts in the primary sensorimotor cortex of the lesioned hemisphere is significantly correlated with improvement of 10 m walk time after VRET (r = −0.719).

Conclusions

We observed improved walking and increased activation in cortical regions of stroke survivors after VRET training. Moreover, the cortical recruitment was associated with better walking function. Our study suggests that cortical networks could be a site of plasticity, and their recruitment may be one mechanism of training-induced recovery of gait function in stroke. This trial is registered with ChiCTR-IOC-15006064.

1. Introduction

Gait impairment is a common consequence of stroke, and the decreases in gait velocity, stride length, and cadence are hallmark features of gait pattern alterations in stroke survivors [12]. Previous studies found that early intervention with physical therapy and gait training to restore walking after stroke was recommended to improve motor function and decrease disability [34]. As gait impairments are a result of deficient neuromuscular control, a better understanding of the impact and mechanism of those interventions on gait pattern recovery after stroke is therefore essential.

Environmental factors act as critical determinants for the level of community ambulation of stroke patient [5]. The development of computers has resulted in virtual reality (VR) tools which can create life-like scenarios via visual, auditory, and tactile feedback and can provide subjects with a safe and stimulating learning environment [6]. VR has been increasingly used in poststroke rehabilitation; therapy interventions using VR may improve motor function for those patients [715]. VR system might represent the main neural substrate for relearning or resuming impaired motor functions following stroke. A key challenge in neurorehabilitation is to establish optimal training protocols for the given patient [10]. VR could provide a person with senses of encouragement and accomplishment [1619]. However, two main concerns need to be investigated. What kind of rehabilitation strategies can combine with VR, and what degree for those VR combined rehabilitation strategies can facilitate stroke patients? Recently, motor relearning strategies can be applied in VR-enhanced treadmill (VRET) training by numerous movement repetitions and a multisensory approach to stimulate brain plasticity and patients receive visual feedback which is close to real-life experience [12]. While the positive benefits of VRET exercise on gait speed, cadence, step length, community walking time, and balance have been demonstrated [7911121415], the associated changes of brain activity with this training have not been investigated yet.

Advances in imaging, such as blood oxygenation level-dependent functional magnetic resonance imaging (fMRI), have been allowed for the observation of changes in cerebral plasticity and the exploration of recovery mechanisms. The control of gait involves the planning and execution from multiple cortical areas, such as secondary and premotor cortex [11]. Ankle dorsiflexion is an important kinematic aspect of the gait cycle. Using ankle movement, Enzinger et al. [20] observed increased activation in the unlesioned hemisphere associated with increasing functional impairment of the paretic leg in patients with stroke. fMRI studies of patients after stroke have suggested that VR could increase neural activations in the primary motor areas and improve lateralization of primary sensorimotor cortex (SMC) activity [2123]. We hypothesized that recovery of lower limb function after VRET would be associated with changes in brain activation during ankle dorsiflexion.

Therefore, the primary aim of this preliminary study was to investigate if functional reorganization takes place after VRET in subacute stroke survivors with gait impairment, using fMRI and an ankle dorsiflexion paradigm. Correlation between clinical scale changes after VERT and brain activation alterations was also studied to see the relations of the induction of cortical plasticity and functional recovery in subacute stroke survivors. We hope that the results of the current study could help to understand the mechanism of VRET as an early intervention for gait recovery for stroke.

2. Methods

2.1. Participants

Eight stroke survivors were recruited in this study, aged 41–72 years (mean: 58.38 years) and included 6 males and 2 females (Table 1 and Figure 1). Inclusion criteria: (i) 18 to 80 years in ages; (ii) right-foot dominant; (iii) first incident of ischemic cortical or subcortical stroke which resulted in gait impairment; (iv) stroke was confirmed by MRI within the past 3 months of inclusion; (v) at least 10° of dorsiflexion is available at the ankle. Exclusion criteria: (i) contraindication to MRI scan (implanted medical devices incompatible with MRI testing or claustrophobia); (ii) history of stroke resulted in function impairment; (iii) history of mental disorder or the use of antipsychotic medication; (iv) cognitive impairment (Mini-Mental State Examination score of less than 24 points); (v) unable to speak or hear; (vi) history of recent deep vein thrombosis of the lower limbs; (vii) recent myocardial infarction; (viii) medically unstable; (ix) existing lower extremity pathology. This study was approved by the Ethics Committee of the First Affiliated Hospital of Sun Yat-sen University (SYSU), and all subjects provided informed consent before the experiments.

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Figure 1
Axial structural T1-weighted MRI scans at the level of maximum infarct volume for each patient. And right hemisphere patients flipped on the sagittal axis for better comparison.

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Continue —> Cerebral Reorganization in Subacute Stroke Survivors after Virtual Reality-Based Training: A Preliminary Study

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[Abstract+References] Longitudinal Structural and Functional Differences Between Proportional and Poor Motor Recovery After Stroke

Background. Evolution of motor function during the first months after stroke is stereotypically bifurcated, consisting of either recovery to about 70% of maximum possible improvement (“proportional recovery, PROP”) or in little to no improvement (“poor recovery, POOR”). There is currently no evidence that any rehabilitation treatment will prevent POOR and favor PROP. Objective. To perform a longitudinal and multimodal assessment of functional and structural changes in brain organization associated with PROP. Methods. Fugl-Meyer Assessments of the upper extremity and high-density electroencephalography (EEG) were obtained from 63 patients, diffusion tensor imaging from 46 patients, at 2 and 4 weeks (T0) and at 3 months (T1) after stroke onset. Results. We confirmed the presence of 2 distinct recovery patterns (PROP and POOR) in our sample. At T0, PROP patients had greater integrity of the corticospinal tract (CST) and greater EEG functional connectivity (FC) between the affected hemisphere and rest of the brain, in particular between the ventral premotor and the primary motor cortex. POOR patients suffered from degradation of corticocortical and corticofugal fiber tracts in the affected hemisphere between T0 and T1, which was not observed in PROP patients. Better initial CST integrity correlated with greater initial global FC, which was in turn associated with less white matter degradation between T0 and T1. Conclusions. These findings suggest links between initial CST integrity, systems-level cortical network plasticity, reduction of white matter atrophy, and clinical motor recovery after stroke. This identifies candidate treatment targets.

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via Longitudinal Structural and Functional Differences Between Proportional and Poor Motor Recovery After StrokeNeurorehabilitation and Neural Repair – Adrian G. Guggisberg, Pierre Nicolo, Leonardo G. Cohen, Armin Schnider, Ethan R. Buch, 2017

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[ARTICLE] Plasticity induced by non-invasive transcranial brain stimulation: A position paper – Full Text

Abstract

Several techniques and protocols of non-invasive transcranial brain stimulation (NIBS), including transcranial magnetic and electrical stimuli, have been developed in the past decades. Non-invasive transcranial brain stimulation may modulate cortical excitability outlasting the period of non-invasive transcranial brain stimulation itself from several minutes to more than one hour. Quite a few lines of evidence, including pharmacological, physiological and behavioral studies in humans and animals, suggest that the effects of non-invasive transcranial brain stimulation are produced through effects on synaptic plasticity. However, there is still a need for more direct and conclusive evidence. The fragility and variability of the effects are the major challenges that non-invasive transcranial brain stimulation currently faces. A variety of factors, including biological variation, measurement reproducibility and the neuronal state of the stimulated area, which can be affected by factors such as past and present physical activity, may influence the response to non-invasive transcranial brain stimulation. Work is ongoing to test whether the reliability and consistency of non-invasive transcranial brain stimulation can be improved by controlling or monitoring neuronal state and by optimizing the protocol and timing of stimulation.

1. Introduction

Transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS) are the most commonly used methods of non-invasive transcranial brain stimulation that has been abbreviated by previous authors as either as NIBS or NTBS. Here we use NIBS since it seems to be the most common term at the present time. When it was first introduced in 1985, TMS was employed primarily as a tool to investigate the integrity and function of the human corticospinal system (Barker et al., 1985). Single pulse stimulation was used to elicit motor evoked potentials (MEPs) that were easily evoked and measured in contralateral muscles (Rothwell et al., 1999). The robustness and repeatability of measures of conduction time, stimulation threshold and “hot spot” location allowed TMS to be developed into a standard tool in clinical neurophysiology.

As we review below, a number of NIBS protocols can lead to effects on brain excitability that outlast the period of stimulation. These may reflect basic synaptic mechanisms involving long-term potentiation (LTP)- or long-term depression (LTD)-like plasticity, and because of this there has been great interest in using the methods as therapeutic interventions in neurological and psychiatric diseases. Furthermore, recently they are more frequently applied to modify memory processes and to enhance cognitive function in healthy individuals. However, apart from success in treating some patients with depression (Lefaucheur et al., 2014; Padberg et al., 2002, 1999), there is little consensus that they have improved outcomes in a clinically meaningful fashion in any other conditions. The reason for this is probably linked to the reason why many other protocols failed to reach routine clinical neurophysiology: they are too variable both within and between individuals to make them practically useful in a health service setting (Goldsworthy et al., 2014; Hamada et al., 2013; Lopez-Alonso et al., 2014, 2015).

Below we review the evidence for the mechanisms underlying the “neuroplastic” effects of NIBS, and then consider the problems in reproducibility and offer some potential ways forward in research. […]

Continue —> Plasticity induced by non-invasive transcranial brain stimulation: A position paper – ScienceDirect

There are three major lines of evidence supporting NIBS produces effects…

Fig. 1. There are three major lines of evidence supporting NIBS produces effects through mechanisms of synaptic plasticity: (1) Drugs that modulate the function of critical receptors/channels for plasticity, e.g. Ca2+ channels and NMDA receptors, alter the effect of NIBS; (2) NIBS mainly changes I-waves rather than the D-wave in the epidural recording of descending volleys evoked by TMS, suggesting the effect of NIBS occurs trans-synaptically; and (3) NIBS interacts between protocols and with motor practice and cognitive learning processes, suggesting the effect of NIBS is involves in plasticity-related motor and psychological processes.

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[Abstract] Polarity-independent effects of tDCS on paired associative stimulation-induced plasticity

Abstract

Background

Transcranial direct current stimulation (tDCS) can polarize the cortex of the human brain.

Objective

/Hypothesis: We sought to verify the hypothesis that posterior-anterior (PA) but not anterior-posterior (AP) tDCS of primary motor cortex (M1) produces cooperative effects with corticospinal plasticity induced by paired associative stimulation of the supplementary motor area (SMA) to M1 projection (PASSMA→M1) in a highly controlled experimental design.

Methods

Three experimental conditions were tested in a double-blinded, randomized crossover design in 15 healthy adults: Navigated PASSMA→M1 during PA-tDCS (35 cm2 electrodes, anode 3 cm posterior to M1 hand area, cathode over contralateral frontopolar cortex, 1 mA, 2 × 5 min) or AP-tDCS (reversed polarity), or sham-tDCS. Effects were analyzed over 120 min post-intervention by changes of motor evoked potential (MEP) amplitude in a hand muscle.

Results

There was no significant effect of tDCS on PASSMA→M1 induced plasticity in the repeated-measures ANOVA. However, post-hoc within-subject contrasts revealed a significant tDCS with PASSMA→M1 interaction. This was explained by PA-tDCS and AP-tDCS modifying the PASSMA→M1 effect into the same direction in 13/15 subjects (87%, p = 0.004 for deviation from equality). Sizes of the PA-tDCS and AP-tDCS effects were correlated (rs = 0.53, p = 0.044). A control experiment demonstrated that PA-tDCS and AP-tDCS alone (without PASSMA→M1) had no effect on MEP amplitude.

Conclusions

Data point to unidirectional tDCS effects on PASSMA→M1 induced plasticity irrespective of tDCS polarity, in contrast to our hypothesis. We propose that radial symmetry of cortical columns, gyral geometry of motor cortex, and cooperativity of plasticity induction can explain the findings.

Source: Polarity-independent effects of tDCS on paired associative stimulation-induced plasticity

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[Abstract] Virtual Reality and Serious Games in Neurorehabilitation of Children and Adults: Prevention, Plasticity, and Participation

Use of virtual reality (VR) and serious games (SGs) interventions within rehabilitation as motivating tools for task specific training for individuals with neurological conditions are fast-developing. Within this perspective paper we use the framework of the IV STEP conference to summarize the literature on VR and SG for children and adults by three topics: Prevention; Outcomes: Body-Function-Structure, Activity and Participation; and Plasticity. Overall the literature in this area offers support for use of VR and SGs to improve body functions and to some extent activity domain outcomes. Critical analysis of clients’ goals and selective evaluation of VR and SGs are necessary to appropriately take advantage of these tools within intervention. Further research on prevention, participation, and plasticity is warranted. We offer suggestions for bridging the gap between research and practice integrating VR and SGs into physical therapist education and practice.

Source: Virtual Reality and Serious Games in Neurorehabilitation of… : Pediatric Physical Therapy

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[ARTICLE] Diffusion MRI and the detection of alterations following traumatic brain injury – Full Text

Abstract

This article provides a review of brain tissue alterations that may be detectable using diffusion magnetic resonance imaging MRI (dMRI) approaches and an overview and perspective on the modern dMRI toolkits for characterizing alterations that follow traumatic brain injury (TBI). Noninvasive imaging is a cornerstone of clinical treatment of TBI and has become increasingly used for preclinical and basic research studies. In particular, quantitative MRI methods have the potential to distinguish and evaluate the complex collection of neurobiological responses to TBI arising from pathology, neuroprotection, and recovery. dMRI provides unique information about the physical environment in tissue and can be used to probe physiological, architectural, and microstructural features. Although well-established approaches such as diffusion tensor imaging are known to be highly sensitive to changes in the tissue environment, more advanced dMRI techniques have been developed that may offer increased specificity or new information for describing abnormalities. These tools are promising, but incompletely understood in the context of TBI. Furthermore, model dependencies and relative limitations may impact the implementation of these approaches and the interpretation of abnormalities in their metrics. The objective of this paper is to present a basic review and comparison across dMRI methods as they pertain to the detection of the most commonly observed tissue and cellular alterations following TBI.

1 INTRODUCTION

Despite the long history of traumatic brain injury (TBI) as a prevalent cause of death and disability in humans, defining the neurobiological underpinnings of damage and recovery following TBI remains a central challenge. The complex collection of physiological, cellular, and molecular changes that follow TBI can appear to be remarkably heterogeneous, but at the same time they are highly organized into coordinated responses such as neurodegeneration, inflammation, and regeneration. The corpus of histological studies spanning a variety of experimental animal models of TBI have provided crucial insights about the pathomechanisms and cellular alterations that accompany posttraumatic tissue change, but considerable work remains to determine the spatiotemporal evolution of abnormalities, interrelationships among different tissue responses, and their impact on health and behavioral outcomes. Noninvasive imaging in animal models has the potential to build on what is known from histology by providing longitudinal and whole-brain information, but for this approach to be successful it is essential to first improve the understanding of how imaging abnormalities correspond to tissue and cellular changes.

Diffusion magnetic resonance imaging (dMRI) methods are particularly promising for the development of imaging markers of TBI pathology because they are sensitive to microscale water displacement as a proxy for tissue environment geometry and provide a range of quantitative scalar metrics across the whole brain. Furthermore, dMRI may be combined with other conventional or advanced magnetic resonance imaging (MRI) methods such as arterial spin labeling, susceptibility-weighted imaging, or a variety of contrast agent MRI approaches to provide complementary and comprehensive outcome measures. Standard dMRI methods and especially diffusion tensor imaging (DTI) have already demonstrated sensitive detection of abnormalities in a number of experimental models of TBI. In the past decade, multiple advanced dMRI approaches have extended beyond the conventional models with the goals of improving the physical description of water diffusion (e.g., by modeling “non-Gaussian” diffusion) or parameterizing dMRI with respect to the expected biological environment (e.g., by modeling cellular compartments and/or fiber geometry). These new tools will be valuable if they are able to improve the sensitivity or specificity of dMRI following TBI; however, we lack a systematic understanding of how dMRI methods differ from one another for detecting and describing tissue alterations.

A number of excellent reviews exist to describe the current understanding of cellular mechanisms of TBI in general (Bramlett & Dietrich, 2015; Pekna & Pekny, 2012) and within particular areas of neurobiology including neurodegeneration (Johnson, Stewart, & Smith, 2013; Stoica & Faden, 2010), inflammation (Burda, Bernstein, & Sofroniew, 2016; Ziebell & Morganti-Kossmann, 2010), and myelin changes (Armstrong, Mierzwa, Marion, & Sullivan, 2016), among others. As well, several existing reviews have been published regarding MRI and DTI to study human TBI (Brody, Mac Donald, & Shimony, 2015; Duhaime et al., 2010; Hulkower, Poliak, Rosenbaum, Zimmerman, & Lipton, 2013), and recently a pertinent overview and summary of advanced dMRI tools and their relevance to clinical outcomes was published (Douglas et al., 2015). The focus of the present review is to combine what is known from work in experimental models of TBI about tissue and cellular alterations that may affect the physical tissue environment with a comparative description of the major methods for dMRI that may be differentially sensitive to TBI-related tissue change alongside several important caveats for their use and interpretation. The first section provides a categorical summary of cellular response to trauma, emphasizing alterations with microstructural, architectural, or neuroanatomical manifestations that may give rise to detectable dMRI abnormalities, including a review of the existing dMRI studies in experimental TBI models. The second section contains a comparative overview of presently available dMRI methods from standard approaches to advanced techniques. The objective of this article is to provide a reference for the current understanding of these topics as well as a perspective to help guide selection of dMRI tools based on particular aspects of TBI questions.

Continue —> Diffusion MRI and the detection of alterations following traumatic brain injury – Hutchinson – 2017 – Journal of Neuroscience Research – Wiley Online Library

Figure 2. Cross-model comparison of scalar maps in the injured brain. A range of tissue and injury-related contrasts may be visually observed in this collage of 16 representative metrics in the same slice from different dMRI models. This cross-model view of scalar maps demonstrates the potential for nonredundant information about regions of injury that may be gleaned from different models. DTI metrics of fractional anisotropy (FA), trace (TR), axial and radial diffusivity (Dax and Drad), directionally encoded color (DEC) map weighted by lattice index, DEC weighted by Westin linear anisotropy (WL) and DEC weighted by Westin planar anisotropy (WP), DKI metrics of mean kurtosis (MK), axial and radial kurtosis (AK and RK) and kurtosis FA (KFA), MAP-MRI metrics of return to the origin, axis, and plane probabilities (RTOP, RTAP, and RTPP), propagator anisotropy (PA) and non-Gaussianity (NG) and NODDI metrics of compartment volume fractions for isotropic free water (Viso), intracellular water (Vic) and intracellular restricted water (Vir), and orientation dispersion index (ODI). Insets of each map show tissue near the injury site where dMRI values are expected to be abnormal.

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