Cortical Plasticity In Patients Research Articles

Auditory Cortical Plasticity in Patients with Single-Sided Deafness Before and After Cochlear Implantation

PurposeThis study investigated neuroplastic changes induced by postlingual single-sided deafness (SSD) and the effects of a cochlear implantation for the deaf ear. Neural processing of acoustic signals from the normal hearing ear to the brain was studied before and after implantation using a positron emission tomography (PET)/CT scanner.MethodsEight patients with postlingual SSD received a cochlear implant (CI) in a prospective clinical trial. Dynamic imaging was performed in a PET/CT scanner using radioactively labeled water ([15O]H2O) to localize changes in the regional cerebral blood flow (rCBF) with and without an auditory task of logatomes containing speech-like elements without meaningful context. The normal hearing ear was stimulated before implantation and after the use of the cochlear implant for at least 8 months (mean 13.5, range 8.1–26.6). Eight age- and gender-matched subjects with normal hearing on both sides served as healthy control subjects (HCS).ResultsWhen the normal hearing ear of SSD patients was stimulated before CI implantation, the [15O]H2O-PET showed a more symmetrical rCBF in the auditory regions of both hemispheres in comparison to the HCS. The use of CI increased the asymmetry index (AI) in six of eight patients indicating an increase of activity of the contralateral hemisphere. Non-parametric statistics revealed a significant difference in the AI between patients before CI implantation and HCS (p < .01), which disappeared after CI implantation (p = .195).ConclusionThe functional neuroimaging data showed a tendency towards normalization of neuronal activity after CI implantation, which supports the effectiveness of CI in SSD patients.Trial RegistrationClinicalTrials.gov Identifier: NCT01749592, December 13, 2012.

TU-154. Effect of high intensity focused ultrasound induced thalamotomy on long-circuit inhibition and motor cortical plasticity in patients with essential tremor

TU-154. Effect of high intensity focused ultrasound induced thalamotomy on long-circuit inhibition and motor cortical plasticity in patients with essential tremor

A systematic review of TMS and neurophysiological biometrics in patients with schizophrenia.

Background:Transcranial magnetic stimulation can be combined with electromyography (TMS-EMG) and electroencephalography (TMS-EEG) to evaluate the excitatory and inhibitory functions of the cerebral cortex in a standardized manner. It has been postulated that schizophrenia is a disorder of functional neural connectivity underpinned by a relative imbalance of excitation and inhibition. The aim of this review was to provide a comprehensive overview of TMS-EMG and TMS-EEG research in schizophrenia, focused on excitation or inhibition, connectivity, motor cortical plasticity and the effect of antipsychotic medications, symptom severity and illness duration on TMS-EMG and TMS-EEG indices.Methods:We searched PsycINFO, Embase and Medline, from database inception to April 2020, for studies that included TMS outcomes in patients with schizophrenia. We used the following combination of search terms: transcranial magnetic stimulation OR tms AND interneurons OR glutamic acid OR gamma aminobutyric acid OR neural inhibition OR pyramidal neurons OR excita* OR inhibit* OR GABA* OR glutam* OR E-I balance OR excitation-inhibition balance AND schizoaffective disorder* OR Schizophrenia OR schizophreni*.Results:TMS-EMG and TMS-EEG measurements revealed deficits in excitation or inhibition, functional connectivity and motor cortical plasticity in patients with schizophrenia. Increased duration of the cortical silent period (a TMS-EMG marker of γ-aminobutyric acid B receptor activity) with clozapine was a relatively consistent finding.Limitations:Most of the studies used patients with chronic schizophrenia and medicated patients, employed cross-sectional group comparisons and had small sample sizes.Conclusion:TMS-EMG and TMS-EEG offer an opportunity to develop a novel and improved understanding of the physiologic processes that underlie schizophrenia and to assess the therapeutic effect of antipsychotic medications. In the future, these techniques may also help predict disease progression and further our understanding of the excitatory/inhibitory balance and its implications for mechanisms that underlie treatment-resistant schizophrenia.

Altered motor cortical plasticity in patients with hepatic encephalopathy: A paired associative stimulation study

ObjectiveHepatic encephalopathy (HE) is a potentially reversible brain dysfunction caused by liver failure. Altered synaptic plasticity is supposed to play a major role in the pathophysiology of HE. Here, we used paired associative stimulation with an inter-stimulus interval of 25 ms (PAS25), a transcranial magnetic stimulation (TMS) protocol, to test synaptic plasticity of the motor cortex in patients with manifest HE. Methods23 HE-patients and 23 healthy controls were enrolled in the study. Motor evoked potential (MEP) amplitudes were assessed as measure for cortical excitability. Time courses of MEP amplitude changes after the PAS25 intervention were compared between both groups. ResultsMEP-amplitudes increased after PAS25 in the control group, indicating PAS25-induced synaptic plasticity in healthy controls, as expected. In contrast, MEP-amplitudes within the HE group did not change and were lower than in the control group, indicating no induction of plasticity. ConclusionsOur study revealed reduced synaptic plasticity of the primary motor cortex in HE. SignificanceReduced synaptic plasticity in HE provides a link between pathological changes on the molecular level and early clinical symptoms of the disease. This decrease may be caused by disturbances in the glutamatergic neurotransmission due to the known hyperammonemia in HE patients.

Cortical plasticity assessment predicts decline in patients with mild cognitive impairment

AbstractBackgroundAlzheimer`s disease (AD) is characterized by loss of synaptic connections, cell death and disruption of structural and functional networks. One of the most consistent findings is the impairment of cortical plasticity, especially Long Term Potentiation (LTP) mechanisms. Recently, the use of new diagnostic criteria allowed to considered AD as a clinico‐biological entity identifiable in vivo on the presence of biomarkers. In light of these new criteria, aim of the current work is to investigate cortical plasticity in patients with hippocampal type memory impairment admitted for the first time in the memory clinic and stratified according to CSF biomarkers profile; moreover we followed patients up to a period of three years to explore the relationship between neurophysiological, neuropsychological and CSF biomarkers and clinical progression.MethodSeventy‐three patients were recruited and followed up for 36 months. They underwent CSF sampling and Transcranial Magnetic Stimulation to investigate LTP and intracortical circuits. According to the new AD criteria we divided patients in three groups: 1) Mild Cognitive Impaired (MCI) patients (n=21); Prodromal AD (PROAD) patients (n=24); AD Dementia (ADD) patients (n=28).ResultIn neurophysiological evaluations only iTBS protocol was different among the different groups showing a paradoxical reversal of LTP for ADD and PROAD and a poor response for MCI patients. ProAD worsened faster than MCI. Regression analyses showed that LTP impairment was related to clinical progression. Kaplan‐Meyer analyses showed that patients expressing the worst LTP values were the ones to progress faster in a 3 year time.ConclusionThe new criteria based on the presence of biomarkers and dementia allow us to identify patients at a prodromal stage that will develop dementia due to AD. LTP impairment drives the clinical progression in patients at prodromal stages confirming its pivotal role in determining cognitive decline. These results pave the way for the identification of new therapeutic targets such as synaptic plasticity modulators.

Decreased medial entorhinal cortical thickness in olanzapine exposed female rats is not ameliorated by exercise

Aerobic exercise has been associated with hippocampal plasticity, both in healthy adults and in psychosis patients, but its impact on cortical regions remains unclear. The entorhinal cortex serves as a critical gateway for the hippocampus, and recent studies suggest that this region may also be impacted following an exercise regime. In order to investigate the effects of antipsychotic medications and exercise on the entorhinal cortex, female rats were chronically administered either olanzapine or vehicle and were either sedentary or had access to a running wheel for 9 weeks. Olanzapine-treated rats had decreased medial entorhinal cortical thickness compared to vehicle-treated rats. A statistically significant interaction was observed for layer II of the entorhinal cortex, with exercising rats having significantly greater thickness compared to sedentary rats in the vehicle group, but not the olanzapine group. Greater total entorhinal and lateral entorhinal cortical thickness was associated with greater average activity. In exercising rats, decreasing glucose intolerance was associated with larger total entorhinal and layer II cortical thickness. Lower fasting insulin levels were associated with greater total entorhinal, lateral entorhinal, and layer II cortical thickness. The relationship between increased activity and greater entorhinal cortical thickness was mediated by reduced fasting insulin, indicating that regulation of metabolic risk factors may contribute to impact of aerobic exercise on the entorhinal cortex. Aerobic exercise may be helpful in counteracting metabolic side effects of antipsychotic medications and managing these side effects may be key to promoting entorhinal cortical plasticity in patients treated with second-generation antipsychotic drugs.

Abnormal intrinsic functional activity in patients with cervical spondylotic myelopathy: a resting-state fMRI study.

PurposeWe employed resting-state fMRI analyses to reveal central functional reorganization in the brains of patients with cervical spondylotic myelopathy (CSM) and to provide complementary evidence of cortex reorganization in these patients.Patients and methodsWe obtained Fisher’s z transformation amplitude of low-frequency fluctuations (zALFF) and Fisher’s z transformation regional homogeneity (zReHo) measurements from 33 patients with CSM and 33 healthy controls (HC) and used the brain regions with significant alterations in the zALFF or zReHo values as seed regions. Then, we calculated Pearson’s correlation coefficients between the resting-state time courses of each seed and the time series of the rest of the brain. Lastly, we computed correlations between the altered zALFF, zReHo, and functional connectivity with Japanese Orthopaedic Association scores, Neck Disability Index score, and the duration of symptoms in patients with CSM.ResultszALFF and zReHo values were increased in the left medial superior frontal gyrus (lSFGmed) and left supramarginal gyrus (lSMG) in patients with CSM compared with those in the HC group. Selecting lSFGmed as the seed, we observed increased functional connectivity between it and the left postcentral gyrus (lPoCG) and left rolandic operculum and decreased functional connectivity with the right medial superior frontal gyrus in patients with CSM. In addition, there was a significant increase in the functional connectivity between the lSMG (seed) and the left calcarine and lPoCG in patients with CSM. However, we did not find any significant correlation between the resting-state findings and the clinical performance of patients with CSM.ConclusionThese observed intrinsic functional changes in the patients with CSM may be related to functional reorganization and reflect the innate cortical plasticity in patients with CSM. Notably, the increased connectivity between the lPoCG and the two seed ROIs indicates the adaptive changes in patients with CSM. These findings provide complementary evidence of cortex reorganization in CSM.

Cortical plasticity in patients with median nerve lesions studied with MEG

We have previously shown age- and time-dependent effects on brain activity in the primary somatosensory cortex (SI), in a functional magnetic resonance imaging (fMRI) study of patients with median nerve injury. Whereas fMRI measures the hemodynamic changes in response to increased neural activity, magnetoencephalography (MEG) offers a more concise way of examining the evoked response, with superior temporal resolution. We therefore wanted to combine these imaging techniques to gain additional knowledge of the plasticity processes in response to median nerve injury. Nine patients with median nerve trauma at the wrist were examined with MEG. The N1 and P1 responses at stimulation of the injured median nerve at the wrist were lower in amplitude compared to the healthy side (p < .04). Ulnar nerve stimulation of the injured hand resulted in larger N1 amplitude (p < .04). The amplitude and latency of the response did not correlate with the sensory discrimination ability. There was no correlation between N1 amplitude and size of cortical activation in fMRI. There was no significant difference in N1 latency between the injured and healthy median nerve. N1 latency correlated positively with age in both the median and ulnar nerve, and in both the injured and the healthy hand (p < .02 or p < .001). It is concluded that conduction failure in the injured segment of the median nerve decreases the amplitude of the MEG response. Disinhibition of neighboring cortical areas may explain the increased MEG response amplitude to ulnar nerve stimulation. This can be interpreted as a sign of brain plasticity.

Adaptive and Maladaptive Neural Plasticity Due to Facial Nerve Palsy

Abstract. This paper reviews adaptive and maladaptive mechanisms of cortical plasticity in patients suffering from peripheral facial palsy. As the peripheral facial nerve is a pure motor nerve, a facial nerve lesion is causing an exclusive deefferentation without deafferentation. We focus on the question of how the investigation of pure deefferentation adds to our current understanding of brain plasticity which derives from studies on learning and studies on brain lesions. The importance of efference and afference as drivers for cortical plasticity is discussed in addition to the crossmodal influence of different competitive sensory inputs. We make the attempt to integrate the experimental findings of the effects of pure deefferentation within the theoretical framework of cortical responses and predictive coding. We show that the available experimental data can be explained within this theoretical framework which also clarifies the necessity for maladaptive plasticity. Finally, we propose rehabilitation approaches for directing cortical reorganization in the appropriate direction and highlight some challenging questions that are yet unexplored in the field.

Cortical Plasticity Induction by Pairing Subthalamic Nucleus Deep-Brain Stimulation and Primary Motor Cortical Transcranial Magnetic Stimulation in Parkinson's Disease.

We introduced a new experimental paradigm to test the hypothesis that pairing subthalamic nucleus deep-brain stimulation (STN-DBS) with motor cortical transcranial magnetic stimulation (M1-TMS) at specific times can induce cortical plasticity in patients with Parkinson's disease (PD). We found that repeated pairing of STN-DBS with TMS at short (∼ 3 ms) and medium (∼ 23 ms) intervals increased cortical excitability that lasted for up to 45 min, whereas the control condition (fixed latency of 167 ms) had no effects on cortical excitability. This is the first demonstration of associative plasticity in the STN-M1 circuits in PD patients using this novel technique. The potential therapeutic effects of combining DBS and noninvasive cortical stimulation should be investigated further.

Transcranial Direct Current Stimulation for the Treatment of Refractory Symptoms of Schizophrenia. Current Evidence and Future Directions.

Schizophrenia is a severe and frequent neuropsychiatric disorder. Despite antipsychotic medications, up to 30% of patients with schizophrenia still report disabling treatment-resistant symptoms. Transcranial direct current stimulation (tDCS) has been proposed as a novel method to alleviate such symptoms. Here, we review studies investigating the effects of tDCS on symptoms, cognition, brain activity and cortical plasticity in patients with schizophrenia. We provide an up-to-date and comprehensive overview of the use of tDCS in patients with schizophrenia. More specifically, we first present the effects of tDCS on treatment-resistant symptoms of schizophrenia. We report that tDCS applied over the frontotemporal regions reduced auditory hallucinations, with a mean 34% reduction of symptoms. Moreover, tDCS applied over both prefrontal cortices reduced negative symptoms and catatonia. We discuss the need for further sham-controlled studies to confirm these effects. Second, we present the impact of tDCS on cognitive functions in patients with schizophrenia. Positive effects of tDCS have been reported on learning, working memory, attention and source-monitoring. Third, we review the effects of tDCS on brain activity in patients with schizophrenia. Although only few studies investigated the effects of tDCS using neuroimaging technics, these studies are helpful at identifying the mechanisms of action of tDCS in schizophrenia. Fourth, we present tDCS studies on cortical plasticity showing reduced cortical plasticity in patients with schizophrenia that tDCS may beneficially modulate. Lastly, we discuss the safety aspects of tDCS in patients with schizophrenia and potential directions to improve efficacy for this clinical populations.

Cortical plasticity in patients with Parkinson's disease a window for therapeutic non-invasive neuromodulation.

Several evidences in animal models have consistently an alteration of cortico-striatal plasticity, which is related to the degeneration of the substantia nigra. An alteration of plasticity have also been reported in humans by recording evoked field potentials in the substantia nigra pars reticulata of PD patients undergoing subthalamic nucleus (STN) stimulation where high-frequency (HF) in the OFF state did not induce a lasting change in field potential amplitude in the substantia nigra. In addition protocols of non-invasive brain stimulation, such as paired associative stimulation (PAS) and theta-burst stimulation (TBS), can be used to investigate cortical plasticity of the human primary motor cortex. Despite data reported in literature are apparently controversial with some studies showing a reduced or increased or even normal LTP and LTD like plasticity, recent evidences suggest the hypothesis that these different pat- terns of cortical plasticity likely depend on the stage of the disease and on the concomitant administration of L-DOPA. The current review will provide an up-to-date of these issues on cortical plasticity in PD discussing the clinical implications in rehabilitation. In addition in the last section we will review the state of art of non invasive neuro- modulation as adjuvant treatment in the advanced stage of the disease.

EPA-1506 – Impact of brain-derived neurotrophic factor (BDNF) gene polymorphism on cortical inhibition in schizophrenia

Neuronal plasticity is a characteristic feature of the human central nervous system. Impaired cortical plasticity has been reported to be associated with a val/met gene-polymorphism in the brain-derived neurotrophic factor (BDNF) gene. Based on former studies, impaired cortical plasticity has been described as a common, yet not fully understood phenomenon in patients with schizophrenia. The aim of the study was to investigate the impact of the val/met-BDNF gene-polymorphism on cortical plasticity in patients with schizophrenia. Cortical plasticity was investigated in a cross-sectional sample of schizophrenia patients (SZ) and healthy controls (HC) using anodal and cathodal transcranial direct current stimulation (tDCS) applied to the primary motor cortex inducing long-term potentiation (LTP) and depression (LTD). The after-effect of the applied tDCS was then probed by TMS before and after tDCS stimulation. TMS in all participants was conducted using a standard 70 mm-TMS figure-of-eight magnetic coil connected to a MagPro X 100 magnetic stimulator. Analyses were focused on resting-motor threshold (RMT), 1mV motor-evoked potential (MEP), short-interval intracortical inhibition (SICI at 3 ms), intracortical facilitation (ICF at 12 ms) and cortical silent period (CSP at 120% RMT). The statistical analyses included n=43 SZ and n=44 HC participants (all numbers presented under reserve of further examination) thus resulting in the largest available sample to probe cortical plasticity parameters in BDNF-genotyped schizophrenia patients. Further results will be presented at the conference. The findings will give new insights into the influence of plasticity-associated gene polymorphisms and the pathophysiology of schizophrenia.

Repetitive transcranial magnetic stimulation for clinical applications in neurological and psychiatric disorders: an overview.

Neurological and psychiatric disorders are characterized by several disabling symptoms for which effective, mechanism-based treatments remain elusive. Consequently, more advanced non-invasive therapeutic methods are required. A method that may modulate brain activity and be viable for use in clinical practice is repetitive transcranial magnetic stimulation (rTMS). It is a non-invasive procedure whereby a pulsed magnetic field stimulates electrical activity in the brain. Here, we focus on the basic foundation of rTMS, the main stimulation parametters, the factors that influence individual responses to rTMS and the experimental advances of rTMS that may become a viable clinical application to treat neurological and psychiatric disorders. The findings showed that rTMS can improve some symptoms associated with these conditions and might be useful for promoting cortical plasticity in patients with neurological and psychiatric disorders. However, these changes are transient and it is premature to propose these applications as realistic therapeutic options, even though the rTMS technique has been evidenced as a potential modulator of sensorimotor integration and neuroplasticity. Functional imaging of the region of interest could highlight the capacity of rTMS to bring about plastic changes of the cortical circuitry and hint at future novel clinical interventions. Thus, we recommend that further studies clearly determine the role of rTMS in the treatment of these conditions. Finally, we must remember that however exciting the neurobiological mechanisms might be, the clinical usefulness of rTMS will be determined by its ability to provide patients with neurological and psychiatric disorders with safe, long-lasting and substantial improvements in quality of life.

7. Cortical plasticity in patients with l-dopa induced dyskinesias

Objective: Effects of PAS 25 protocol in PD patients with l -dopa induced dyskinesias (LID). Subjects and methods: We analyzed 10 patients with PD who had dyskinesias as a side effect of l -dopa therapy and 10 healthy subjects in control group (CG). Plasticity and excitability of the hand primary motor cortex of the more affected side were evaluated using transcranial magnetic stimulation (TMS) techniques. Recording was done before (Tb), immediately (T0) and 30 min after procedure (T30). Patients were tested in “off” and “on” states. Results: There was no difference for MEP between groups. Patients with l -dopa induced dyskinesias with medication immediately after PAS, showed decrease of slope at higher levels of stimulation (150% rMT, p = 0.058) compared with CG. All subjects show a decrease of SP ( p p = 0.034) compared with CG, without significance for ICF ( p = 0.578), regardless of the applied procedures. Conclusion: Patients with LID have a higher inhibition, probably due to involuntary movements. It is possible that their brain is “working” at smaller scale. PAS 25 protocols had no significant effect on cortical plasticity in patients with PD who have LID.

Reperfusion Does Not Improve Impaired Rapid-Onset Cortical Plasticity in Patients with Severe Stenosis of the Internal Carotid Artery

BackgroundSevere stenosis of the internal carotid artery (ICA) has been associated with impaired cognition in patients, but its effect on rapid-onset cortical plasticity is not known. Carotid endarterectomy (CEA) in patients with severe ICA stenosis reduces stroke risk, but the impact on cognition or physiology of the respective hemisphere remains controversial.Methods/Results16 patients with severe stenosis of the ICA and 16 age and sex matched controls were included. Rapid-onset cortical plasticity was assessed using the paired-associative stimulation (PAS) protocol. PAS models long-term synaptic potentiation in human motor cortex, combining repetitive stimulation of the peripheral ulnar nerve with transcranial magnetic stimulation of the contralateral motor cortex. Cognitive status was assessed with a neuropsychological test battery. In patients, verbal learning and rapid-onset cortical plasticity were significantly reduced as compared to controls. Identical follow-up tests in 9 of the 16 patients six months after CEA revealed no improvement of cognitive parameters or cortical plasticity.ConclusionsDecreased rapid-onset cortical plasticity in patients with severe stenosis of the ICA was not improved by reperfusion. Thus, other strategies known to increase plasticity should be tested for their potential to improve cortical plasticity and subsequently cognition in these patients.

Precise temporal association between cortical potentials evoked by motor imagination and afference induces cortical plasticity

In monkeys, the repeated activation of somatosensory afferents projecting onto the motor cortex (M1) has a pivotal role in motor skill learning. Here we investigate if sensory feedback that is artificially generated at specific times during imagination of a dorsiflexion task leads to reorganization of the human M1. The common peroneal nerve was stimulated to generate an afferent volley timed to arrive during specific phases of the cortical potential generated when a movement was imagined (50 repetitions). The change in the output of M1 was quantified by applying single transcranial magnetic stimuli to the area of M1 controlling the tibialis anterior muscle. The results demonstrated that the concomitance between the cognitive process of movement (motor imagination) and the ascending volley due to the peripheral nerve stimulation can lead to significant increases in cortical excitability. These increases were critically dependent on the timing between the peripherally generated afferent volley and the cortical potential generated during the imagined movement. Only if the afferent volley arrived during the peak negative deflection of the potential, were significant alterations in motor cortical output attained. These results demonstrate that an artificially generated signal (the peripheral afferent volley) can interact with a physiologically generated signal in humans leading to plastic changes within the M1, the final output stage for movement generation within the human brain. The results presented may have implications in systems for artificially inducing cortical plasticity in patients with motor impairments (neuromodulation).

Methods of Assessment of Cortical Plasticity in Patients Following Amputation, Replantation, and Composite Tissue Allograft Transplantation

The brain is always adapting to new inputs from the environment. New noninvasive techniques are available to scrupulously study cortical plasticity. Several studies have proven that these modifications of neural pathways occur because of denervation from injury such as amputation. Changes that occur rapidly are likely because of unmasking of established synapses that are latent, whereas changes that occur over long periods of time are more likely because of establishment of new neural connections. Cortical reorganization that occurs from traumatic amputation has been shown to be reversible with replantation and transplantation. With the new field of composite tissue transplantation, such as hand or face, it is critical to be aware of these changes to choose potential patients and to modify their rehabilitation, on the basis of our understanding of the cortical reorganization that occurs over time.

Non-invasive brain mapping of motor-related areas of four limbs in patients with clinically isolated syndrome compared to healthy normal controls

Functional MRI studies on patients with multiple sclerosis (MS) have demonstrated widespread cortical reorganization of the motor network. However, few functional studies have addressed cortical plasticity in patients with clinically isolated syndrome (CIS). The activity of the lower limb motor system, despite its highlighted involvement in patients with CIS and MS, has been little studied. Thus, brain activation was compared in CIS patients with clinically intact motor systems with that in healthy control participants while they were performing motor tasks with four limbs. A total of 26 right-handed patients with CIS with clinically intact motor systems and 28 right-handed age and sex-matched controls participated in the functional MRI (fMRI) motor task. Patients with CIS showed greater activation in the ipsilateral secondary somatosensory cortex, cingulate gyrus and precuneus cortex while performing the ankle movement task compared to healthy controls. In the finger-tapping task, patients with CIS showed greater activity in the contralateral thalamus, ipsilateral premotor and superior temporal gyrus. In addition, the left inferior frontal gyrus was activated more in patients with CIS, regardless of the hand used. Therefore, despite having clinically intact motor systems, patients with CIS had different motor networks. All novel recruited regions were adjacent to the somatotopy of the primary motor areas of the limbs. Our finding confirm that brain reorganization precedes clinical manifestation, as no patient had any clinical manifestation that suggested involvement of the motor system.

Focal cortical plasticity in patients with high-grade stenosis of the internal carotid artery

Focal cortical plasticity in patients with high-grade stenosis of the internal carotid artery