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Magnetic resonance–guided focused ultrasound (MRgFUS) has been applied successfully in treating refractory tremors in Parkinson disease (PD). It generates a precise thermal ablation in a specific nucleus or tract, such as ventral intermediate nucleus (VIM) or pallidothalamic tract (PTT). Despite a single lesion improving parts of the PD symptoms, the feasibility and efficacy of a stepwise dual-lesion in VIM and PTT are yet to be explored. Three patients with tremor-dominant PD (aged 60.7 ± 6.0 years) received dual-target MRgFUS treatment with a series of primary and secondary outcome measures. The VIM and PTT were navigated based on individual magnetic resonance imaging planning of the brain. The primary outcome measures were the off-status Clinical Rating Scale for Tremor and Unified Parkinson's Disease Rating Scale part III (UPDRS-III). The secondary outcome measures included UPDRS I, II, IV, Hohen and Yahr score, Neuropsychiatry Inventory, Quality of life in PD Rating Scale, Non-Motor Symptoms Scale, and Clinical Global Impression. The baseline data were compared with those acquired 1 day and 1 month following the treatment. The severity of tremor and motor deficits represented by Clinical Rating Scale for Tremor–part B and UPDRS III were significantly improved (P < 0.05 by nonparametric Mann–Whitney U tests) after dual-target ablations. The nonmotor symptoms investigated by UPDRS II and Non-Motor Symptoms Scale also showed significant improvement at the 1-day and 1-month follow-up. There was no adverse effect except temporary procedure-related headache and dizziness during the treatment. Stepwise dual-lesion targeting VIM and PTT is a safe and effective MRgFUS therapeutic strategy for patients with PD. [ABSTRACT FROM AUTHOR]

Objective Previous electrophysiological and psychophysical tests have suggested that somatosensory integration is abnormal in dystonia. Here, we hypothesised that this abnormality could relate to a more general deficit in pre-attentive error/deviant detection in patients with dystonia. We therefore tested patients with dystonia and healthy subjects using a mismatch negativity paradigm (MMN), where evoked potentials generated in response to a standard repeated stimulus are subtracted from the responses to a rare “odd ball” stimulus. Methods We assessed MMN for somatosensory and auditory stimuli in patients with cervical dystonia and healthy age matched controls. Results We found a significant group ∗ oddball type interaction effect (F (1, 34) = 4.5, p  = 0.04, ρ I  = 0.63). A follow up independent t -test for sMMN data, showed a smaller sMMN amplitude in dystonic patients compared to controls (mean difference control-dystonia: −1.0 µV ± 0.3, p  < 0.00, t  = −3.1). However the amplitude of aMMN did not differ between groups (mean difference control-dystonia: −0.2 µV ± 0.2, p  = 0.24, t  = −1.2). We found a positive correlation between somatosensory MMN and somatosensory temporal discrimination threshold. Conclusion These results suggest that pre-attentive error/deviant detection, specifically in the somatosensory domain, is abnormal in dystonia. This could underlie some previously reported electrophysiological and psychophysical abnormalities of somatosensory integration in dystonia. Significance One could hypothesize a deficit in pre-conscious orientation towards potentially salient signals might lead to a more conservative threshold for decision-making in dystonia. [ABSTRACT FROM AUTHOR]

Background: The primary motor sign of Parkinson's disease is bradykinesia. It has been surprisingly difficult to provide a clear neurobiological mechanism for this fundamental movement deficit in Parkinson's disease. It has been proposed that in healthy individuals the gating of sensory afferents prior to and during movement is an essential step in initiating movement. This down-weighting has been proposed to account for the attenuation of the somatosensory evoked potential following median nerve stimulation at the onset of and during hand movements. The objective of this study was to test whether this sensory attenuation present at movement onset in healthy controls is present in patients with Parkinson's disease.Methods: Eighteen right-handed patients with idiopathic Parkinson's disease and 16 right-handed age-matched healthy participants were studied. Somatosensory evoked potentials were elicited after electrical stimulation of the median nerve at the wrist. Electroencephalograms were recorded over the scalp at 3 sites on according to the International 10-20 System (F3, C3, and P3). Somatosensory evoked potentials were recorded in 2 conditions: at rest and at the onset of movement (a self-paced abduction movement of the right thumb).Results: Off medication, Parkinson's disease patients had no sensory attenuation at movement onset. On medication, sensory attenuation at movement onset was present.Conclusions: We suggest that this preliminary result is consistent with the hypothesis that, a failure in sensory attenuation contributes to the difficulties in movement initiation in Parkinson's disease. [ABSTRACT FROM AUTHOR]

Background: Functional (psychogenic) movement disorders (FMD) have features associated with voluntary movement (e.g. distractibility) but patients report movements to be out of their control. One explanation for this phenomenon is that sense of agency for movement is impaired. The phenomenon of reduction in the intensity of sensory experience when movement is self-generated and a reduction in sensory evoked potentials (SEPs) amplitude at the onset of self-paced movement (sensory attenuation) have been linked to sense of agency for movement. Methods: We compared amplitude of SEPs from median nerve stimulation at rest and at the onset of a self-paced movement of the thumb in 17 patients with FMD and 17 healthy controls. Results: Patients showed lack of attenuation of SEPs at the onset of movement compared to reduction in amplitude of SEPs in controls. FMD patients had significantly different ratios of movement onset to rest SEPs than did healthy controls at each electrode: 0.79 in healthy controls and 1.35 in patients at F3 (t = -4.22, p<0.001), 0.78 in healthy controls and 1.12 at patients C3 (t = -3.15, p = 0.004) and 0.77 in healthy controls and 1.05 at patients P3 (t = -2.88, p = 0.007). Conclusions: Patients with FMD have reduced sensory attenuation as measured by SEPs at onset of self-paced movement. This finding can be plausibly linked to impairment of sense of agency for movement in these patients. [ABSTRACT FROM AUTHOR]

Key points Sensory mismatch negativity is impaired in patients with cerebellar lesions, suggesting that the cerebellum may play an important role in this form of sensory processing., Anodal transcranial direct current stimulation over the right cerebellar hemisphere increased the amplitude of sensory mismatch negativity to stimuli delivered to the right hand while cathodal transcranial direct current stimulation reduced it., The cerebellum appears to be an important node in the network mediating sensory mismatch negativity, and tDCS is a useful method with which to manipulate sensory mismatch negativity for experimental studies., Abstract Appropriate orientation towards potentially salient novel environmental stimuli requires a system capable of detecting change in the sensorium. Mismatch negativity (MMN), an evoked potential calculated by subtracting the response to a standard repeated stimulus and a rare 'oddball' stimulus, is proposed as such a change detection mechanism. It is most widely studied in the auditory domain, but here we chose to explore the mechanism of somatosensory MMN, and specifically its dependence on the cerebellum. We recorded event-related potentials (ERPs) evoked in response to auditory and sensory stimuli from 10 healthy subjects before and after anodal, cathodal and sham transcranial direct current stimulation (tDCS) of the right cerebellar hemisphere. There was a significant increase in peak amplitude of somatosensory MMN after anodal tDCS ( F(1,9) = 8.98, P < 0.02, mean difference anodal pre-post: −1.02 μV) and a significant reduction in peak amplitude of somatosensory MMN after cathodal tDCS ( F(1,9) = 7.15, P < 0.03, mean difference cathodal pre-post: 0.65 μV). The amplitude of auditory MMN was unchanged by tDCS. These results reveal the capability of tDCS to cause bidirectional modulation of somatosensory MMN and the dependence of somatosensory MMN on the cerebellum. [ABSTRACT FROM AUTHOR]

Background: Recent research has highlighted the role of the cerebellum in the pathophysiology of myoclonus-dystonia syndrome as a result of mutations in the ɛ-sarcoglycan gene (DYT11). Specifically, a cerebellar-dependent saccadic adaptation task is dramatically impaired in this patient group.Objectives: The objective of this study was to investigate whether saccadic deficits coexist with impairments of limb adaptation to provide a potential mechanism linking cerebellar dysfunction to the movement disorder within symptomatic body regions.Methods: Limb adaptation to visuomotor (visual feedback rotated by 30°) and forcefield (force applied by robot to deviate arm) perturbations were examined in 5 patients with DYT11 and 10 aged-matched controls.Results: Patients with DYT11 successfully adapted to both types of perturbation. Modelled and averaged summary metrics that captured adaptation behaviors were equivalent to the control group across conditions.Conclusions: DYT11 is not characterized by a uniform deficit in adaptation. The previously observed large deficit in saccadic adaption is not reflected in an equivalent deficit in limb adaptation in symptomatic body regions. We suggest potential mechanisms at the root of this discordance and identify key research questions that need future study. © 2018 International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

Key points We studied the interaction between the primary visual cortex and the primary motor cortex using paired transcranial magnetic stimulation (TMS) with an interstimulus interval (ISI) in the range 12-40 ms., The connection is inhibitory at rest and possibly mediated by inhibitory interneurones in the motor cortex., The effect with an ISI of 40 ms reverses into facilitation during a visuomotor (but not audiomotor) reaction task. By contrast, there is no change in inhibition with an ISI of 18 ms, suggesting that separate pathways can be probed at different ISIs., We conclude that a physiologically relevant occipito-motor connection can be activated by means of TMS. It may contribute to visuomotor integration, as well as being involved in certain types of visual epilepsy. , Abstract The major link between the visual and motor systems is via the dorsal stream pathways from visual to parietal and frontal areas of the cortex. Although the pathway appears to be indirect, there is evidence that visual input can reach the motor cortex at relatively short latency. To shed some light on its neural basis, we studied the visuomotor interaction using paired transcranial magnetic stimulation (TMS). Motor-evoked potentials (MEPs) were recorded from the right first dorsal interosseous in sixteen healthy volunteers. A conditioning stimulus (CS) was applied over the phosphene hotspot of the visual cortex, followed by a test stimulus over the left primary motor cortex (M1) with a random interstimulus interval (ISI) in range 12-40 ms. The effects of paired stimulation were retested during visual and auditory reaction-time tasks (RT). Finally, we measured the effects of a CS on short-interval intracortical inhibition (SICI). At rest, a CS over the occiput significantly ( P < 0.001) suppressed test MEPs with an ISI in the range 18-40 ms. In the visual RT, inhibition with an ISI of 40 ms (but not 18 ms) was replaced by a time-specific facilitation ( P < 0.001), whereas, in the auditory RT, the CS no longer had any effect on MEPs. Finally, an occipital CS facilitated SICI with an ISI of 40 ms ( P < 0.01). We conclude that it is possible to study separate functional connections from visual to motor cortices using paired-TMS with an ISI in the range 18-40 ms. The connections are inhibitory at rest and possibly mediated by inhibitory interneurones in the motor cortex. The effect with an ISI of 40 ms reverses into facilitation during a visuomotor RT but not an audiomotor RT. This suggests that it plays a role in visuomotor integration. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD), a progressive disease that affects movement, is related to dopaminergic neuron degeneration. Tc-99m Trodat-1 brain (TRODAT) single-photon emission computed tomography (SPECT) aids the functional imaging of dopamine transporters and is used for dopaminergic neuron enumeration. Herein, we employed a convolutional neural network to facilitate PD diagnosis through TRODAT SPECT, which is simpler than models such as VGG16 and ResNet50. We retrospectively collected the data of 3188 patients (age range 20–107 years) who underwent TRODAT SPECT between June 2011 and December 2019. We developed a set of functional imaging multiclassification deep learning algorithms suitable for TRODAT SPECT on the basis of the annotations of medical experts. We then applied our self-proposed model and compared its results with those of four other models, including deep and machine learning models. TRODAT SPECT included three images collected from each patient: one presenting the maximum absorption of the metabolic function of the striatum and two adjacent images. An expert physician determined that our model's accuracy, precision, recall, and F1-score were 0.98, 0.98, 0.98, and 0.98, respectively. Our TRODAT SPECT model provides an objective, more standardized classification correlating to the severity of PD-related diseases, thereby facilitating clinical diagnosis and preventing observer bias. [ABSTRACT FROM AUTHOR]

Sturge- Weber syndrome is known to be associated with migraine attacks and prolong aura even without cerebral infarction. We report the case of a 36-year-old woman with type III Sturge- Weber syndrome developing with prolonged left homonymous hemianopsia after an intractable migraine-like headache and becoming a permanent visual field defect at 18-month follow up. By adopting a multimodality imaging study, we suggested that the underlying mechanism of prolonged visual field defect was due to blood flow disturbance and vasogenic leakage under the leptomeningeal angioma combining with atrophy and the damaged integrity of white matter in right occipital lobe. [ABSTRACT FROM AUTHOR]

Patients with Parkinson's disease (PD) suffer from motor and non-motor symptoms; 40% would develop dementia (PD-D). Impaired face and emotion processing in PD has been reported; however, the deficits of face processing in PD-D remain unclear. We investigated three essential aspects of face processing capacity in PD-D, and the associations between cognitive, neuropsychiatric assessments and task performances. Twenty-four PD-D patients (mean age: 74.0 ± 5.55) and eighteen age-matched healthy controls (HC) (mean age: 71.0 ± 6.20) received three computerized tasks, morphing-face discrimination, dynamic facial emotion recognition, and expression imitation. Compared to HC, PD-D patients had lower sensitivity (d') and greater neural internal noises in discriminating faces; responded slower and had difficulties with negative emotions; imitated some expressions but with lower strength. Correlation analyses revealed that patients with advancing age, slow mentation, and poor cognition (but not motor symptoms) showed stronger deterioration in face perception. Importantly, these correlations were absent in the age-matched HC. The present study is among the first few examined face processing in patients with PD-D, and found consistent deficits correlated with advancing age and slow mentation. We propose that face discrimination task could be included as a potential test for the early detection of dementia in PD. [ABSTRACT FROM AUTHOR]

Background: Dystonia is a neurological syndrome typically resulting in abnormal postures. Objectives: We tested the role of physical injury as potential risk factor for development of dystonia using The National Health Insurance Research Database of Taiwan. Methods: We identified 65704 people who were coded in the database as having had peripheral traumatic injuries (ICD-9-CM 807–848 and 860–959) in the year 2000. Patients with traumatic brain or spine injuries were excluded from analysis. We matched them using purposive sampling with 65704 people in the database who had not suffered peripheral trauma. We looked then at the incidence of dystonia occurring at least 1 year from the date of the peripheral trauma until 2011. Psychiatric symptoms (depression and anxiety) and sleeps difficulties have been investigated as potential covariates. Results: We found 189 patients with dystonia (0.28%) in the trauma group, and 52 patients with dystonia (0.08%) in the non-trauma group. Trauma was independently associated with dystonia (adjusted HR = 3.12, 95% CI = 2.30–4.24). The incidence density of dystonia in the trauma group was 2.27 per 10000 person-years, while it was 0.71 per 10000 person-years in the non-trauma group Beyond the peripheral trauma, other variables associated to the incidence of dystonia included female sex, aged 40 years and above, depression and sleep disorders. Conclusion: These data from a large population dataset support traumatic injury as a risk factor for the development of dystonia. [ABSTRACT FROM AUTHOR]

Objectives: Subjective tinnitus is a phantom sensation experienced without any external source of sound that profoundly impacts the quality of life. Some investigations have claimed that transcranial direct current stimulation (tDCS) reduces tinnitus, but studies on tDCS have demonstrated variable results. This meta-analysis aimed to examine the effect of tDCS on patients with tinnitus. Methods: We searched for articles published through January 5, 2016, in Medline, Cochrane, EMBASE, and Google Scholar using the following keywords: tinnitus, transcranial direct current stimulation, and tDCS. The study outcomes were change in magnitude estimates of loudness (loudness), tinnitus-related distress (distress), and Tinnitus Handicap Inventory (THI). Results: Pooled results demonstrated that tDCS did not have a beneficial effect on loudness (pooled standardized difference in means = 0.674, 95% CI, -0.089 to 1.437, P = .083). Further, the pooled results demonstrated a greater reduction in distress for the tDCS group (pooled standardized difference in means = 0.634, 95% CI, 0.021-1.247, P = .043). Conclusions: We conclude that the pooled results demonstrated a greater reduction in distress for groups treated with tDCS as compared with those administered a sham treatment. [ABSTRACT FROM AUTHOR]

Background: Colonic diverticular disease is a chronic gastrointestinal disorder. Previous studies have suggested that chronic gastrointestinal tract is involved in the pathophysiology of Parkinson's disease.Object: This study investigated the potential link between colonic diverticular disease and risk of Parkinson's disease.Methods: Data in this nationwide population-based cohort study were obtained from the National Health Insurance Research Database. Patients with colonic diverticular disease were identified from among 23.22 million insured Taiwanese residents who had been diagnosed between 2000 and 2005 and were aged ≥20 years (n = 23367). The comparison cohort included patients without colonic diverticular disease, matched by sex, age, and all comorbidities with the colonic diverticular disease patients cohort (n = 23367). Using univariable and multivariable Cox proportional hazard regression models, we estimated the adjusted hazard ratio (aHR) for PD with a 95% confidence interval (CI) after adjusting for age, sex, and all of comorbidities.Results: The risk of Parkinson's disease was higher in the CDD cohort than in the comparison cohort (HR = 1.27, 95%CI = 1.10-1.47). Compared with patients aged ≥65 years without CDD, the CDD patients in the equal age group had a 1.25-fold increased risk of PD (95% CI = 1.07-1.46).Conclusion: Colonic diverticular disease may be associated with an increased risk of Parkinson's disease. Thus, the risk of this neurodegenerative disease should be considered in patients with colonic diverticular disease. [ABSTRACT FROM AUTHOR]

Parkinson’s disease (PD) and essential tremor (ET) are characterized with motor dysfunctions. Motor circuit dysfunctions can be complementarily investigated by paired associative stimulation (PAS)-induced long-term potentiation (LTP)-like plasticity and diffusion tensor imaging (DTI) of the corticospinal tract (CST). Three groups of twelve subjects with moderate severity PD, ET with intention tremor and healthy controls (HC) were studied. The primary motor cortex (M1) excitability, measured by motor evoked potential (MEP) amplitude and by short-interval and long-interval intracortical inhibition (SICI and LICI) was compared between the three groups before and after PAS. The DTI measures of fractional anisotropy (FA) and mean diffusivity (MD) were acquired. PAS effects and DTI data were simultaneously examined between groups. PAS increased MEP amplitude in HC but not in PD and ET. SICI and LICI were significantly reduced after PAS irrespective of groups. No significant differences of the mean FA and MD were found between groups. There was no significant correlation between the PAS effects and the DTI measures. Findings suggest that both PD and ET with intention tremor have impairment of the associative LTP-like corticospinal excitability change in M1. The microstructure of the CST is not relevant to the deficiency of M1 associative plasticity in PD and ET. [ABSTRACT FROM AUTHOR]

Objective: To compare the strength-duration (S-D) time constants of motor cortex structures activated by current pulses oriented posterior-anterior (PA) or anterior-posterior (AP) across the central sulcus. Methods: Motor threshold and input-output curve, along with motor evoked potential (MEP) latencies, of first dorsal interosseus were determined at pulse widths of 30, 60, and 120 μs using a controllable pulse parameter (cTMS) device, with the coil oriented PA or AP. These were used to estimate the S-D time constant and we compared with data for responses evoked by cTMS of the ulnar nerve at the elbow. Results: The S-D time constant with PA was shorter than for AP stimulation (230.9 ± 97.2 vs. 294.2 ± 90.9 μs; p < 0.001). These values were similar to those calculated after stimulation of ulnar nerve (197 ± 47 μs). MEP latencies to AP, but not PA stimulation were affected by pulse width, showing longer latencies following short duration stimuli. Conclusion: PA and AP stimuli appear to activate the axons of neurons with different time constants. Short duration AP pulses are more selective than longer pulses in recruiting longer latency corticospinal output. Significance: More selective stimulation of neural elements may be achieved by manipulating pulse width and orientation. [ABSTRACT FROM AUTHOR]

Task-specific dystonia is a neurological movement disorder that abnormal contractions of muscles result in the twisting of fixed postures or muscle spasm during specific tasks. Due to the rareness and the pathophysiology of the disease, there is no test to confirm the diagnosis of task-specific dystonia, except comprehensive observations by the experts. Evidence from neural electrophysiological data suggests that enhanced low frequency (4–12 Hz) oscillations in the subcortical structure of the globus pallidus were associated with the pathological abnormalities concerning β and γ rhythms in motor areas and motor cortical network in patients with task-specific dystonia. However, whether patients with task-specific dystonia have any low-frequency abnormalities in motor cortical areas remains unclear. In this study, we hypothesized that low-frequency abnormalities are present in core motor areas and motor cortical networks in patients with task-specific dystonia during performing the non-symptomatic movements and those low-frequency abnormalities can help the diagnosis of this disease. We tested this hypothesis by using EEG, effective connectivity analysis, and a machine learning method. Fifteen patients with task-specific dystonia and 15 healthy controls were recruited. The machine learning method identified 8 aberrant movement-related network connections concerning low frequency, β and γ frequencies, which enabled the separation of the data of patients from those of controls with an accuracy of 90%. Importantly, 7 of the 8 aberrant connections engaged the premotor area contralateral to the affected hand, suggesting an important role of the premotor area in the pathological abnormities. The patients exhibited significantly lower low frequency activities during the movement preparation and significantly lower β rhythms during movements compared with healthy controls in the core motor areas. Our findings of low frequency- and β-related abnormalities at the cortical level and aberrant motor network could help diagnose task-specific dystonia in the clinical setting, and the importance of the contralesional premotor area suggests its diagnostic potential for task-specific dystonia. • Low-frequency was abnormal in the cortical motor areas and network in TSD. • The frequency-related oscillations can help diagnose TSD with an accuracy of 90%. • Contralesional premotor area plays an important role in TSD. [ABSTRACT FROM AUTHOR]

Robot-assisted gait training (RAGT) systems offer the advantages of standard rehabilitation and provide precise and quantifiable control of therapy. We examined the clinical outcome of RAGT and analyzed the correlations between gait analysis data and event-related desynchronization (ERD) and event-related synchronization (ERS) in patients with chronic stroke. We applied the Berg balance scale (BBS) and analyzed gait parameters and the ERD and ERS of self-paced voluntary leg movements performed by patients with chronic stroke before and after undergoing RAGT. A significant change was observed in BBS (p = 0.011). We also showed preliminary outcomes of changes in gait cycle duration (p = 0.015) and in ipsilesional ERS in the low-beta (p = 0.033) and high-beta (p = 0.034) frequency bands before and after RAGT. In addition, correlations were observed between BBS and ipsilesional ERS in the alpha and low-beta bands (r = −0.52, p = 0.039; r = −0.52, p = 0.040). The study demonstrated that RAGT can improve balance and provided an idea of the possible role of brain oscillation and clinical outcomes in affecting stroke rehabilitation. [ABSTRACT FROM AUTHOR]

Introduction Conventional paired associative stimulation (PAS) consists of repeated pairing of a single electric stimulus at median nerve followed by a transcranial magnetic stimulation (TMS) pulse on the contralateral primary motor cortex (M1) with a specific inter-stimulus interval. It induces associative long-term potentiation (LTP) or depression (LTD)-like plasticity at M1. Attention has been found with a positive influence on such plasticity. In this study we adopt electroacupuncture (EA) to replace the transcutaneous electric stimulation, supposedly drawing a strong attention and enhancing the PAS effect. Methods Eleven healthy, right-handed subjects (aged 23.9 ± 2.2 years, 4 men) were studied. Two hundred and twenty-five pairs of TMS of the left M1 preceded by right EA at acupoint ‘Neiguan’ (Pericardium 6 or PC6, located 2 decimeters proximal from the wrist wrinkle) were respectively applied with an interstimulus interval of individual N20 latency plus 2 ms (N20 + 2) and minus 5 ms (N20-5) with at least one week interval. The paired stimulation was delivered at a rate of 0.25 Hz. Sham TMS with a sham coil was performed to exclude any possible effects from the repetitive low-frequency EA stimulation. M1 excitability was assessed by motor-evoked potential (MEP) recruitment curve with five TMS intensity levels (80–120% resting motor threshold), short-interval intracortical inhibition (SICI), intracortical facilitation (ICF) and cerebellar inhibition (CBI) at the abductor pollicis brevis (APB) muscle of the right hand before and after the EA-M1 PAS. In addition, median nerve somatosensory-evoked potentials (SSEP) and H-reflex were measured to monitor somatosensory and spinal excitability, respectively. Results All subjects successfully completed four sessions of the experiment. There was no significant change of the MEP amplitude after the EA-M1 PAS at five TMS intensities. SICI, ICF, CBI, SSEP and H-reflex were also not significantly changed after the EA-M1 PAS intervention (all P  > 0.05 by paired t -test). Conclusion Transcutaneous electric stimulation replaced by EA is not feasible to induce long-term plasticity-like effect. Complicated sensory afferents evoked by electroacupuncture might hamper instead of enhancing the spike timing dependent motor plasticity in M1. [ABSTRACT FROM AUTHOR]