Cerebral Motor Cortex Research Articles

Establishment of a precise novel brain trauma model in a large animal based on injury of the cerebral motor cortex

BackgroundAnimal models are essential in simulating clinical diseases and facilitating relevant studies. New methodWe established a precise canine model of traumatic brain injury (TBI) based on cerebral motor cortex injury which was confirmed by neuroimaging, electrophysiology, and a series of motor function assessment methods. Twelve beagles were divided into control, sham, and model groups. The cerebral motor cortex was identified by diffusion tensor imaging (DTI), a simple marker method, and intraoperative electrophysiological measurement. Bony windows were designed by magnetic resonance imaging (MRI) scan and DTI. During the operation, canines in the control group were under general anesthesia. The canines were operated via bony window craniotomy and dura mater opening in the sham group. After opening of the bony window and dura mater, the motor cortex was impacted by a modified electronic cortical contusion impactor (eCCI) in the model group. ResultsPostoperative measurements revealed damage to the cerebral motor cortex and functional defects. Comparisons between preoperative and postoperative results demonstrated that the established model was successful. Comparison with existing method(s)Compared with conventional models, this is the first brain trauma model in large animal that was constructed based on injury to the cerebral motor cortex under the guidance of DTI, a simple marker method, and electrophysiology. ConclusionThe method used to establish this model can be standardized to enhance reproducibility and provide a stable and precise large animal model of TBI for clinical and basic research.

High frequency transcranial magnetic stimulation combined with mirror therapy improves upper limb motor function post-stroke

Objective To investigate the effect of repetitive transcranial magnetic stimulation (rTMS) combined with the mirror therapy (MT) on the recovery of upper limb function recovery 3 to 6 months after a stroke. Methods Forty-five male patients were randomly assigned to an MT (A) group, an rTMS+ MT (B) group or an MT+ rTMS group (C ), each of 15. All received conventional medical treatment and stroke rehabilitation. In addition, group A received 60 min of MT daily, 5 days a week for 4 weeks. Group B received 10 min of rTMS over the M1 area of the affected hemisphere followed by 50 min of MT treatment, and group C received 50 min of MT treatment followed by 10 min of rTMS. rTMS was delivered at a frequency of 10 Hz and an intensity of 90% resting motor threshold. The latency of motor evoked potential (MEP) for the affected abductor pollicis brevis muscle and its central motor conduction time (CMCT) were observed before and after the treatment. The upper extremity portion of the Fugl-Meyer assessment (FMA) was performed along with a functional test for the hemiplegic upper extremity (FTHUE). The motricity index (MI) was also quantified. Results Average MEP latency and CMCT had decreased significantly in all three groups after the treatments. The average MEP latency of group B was significantly shorter than that of group A, and CMCT was also significantly shorter than for groups A and C. Moreover, after the intervention, all of the groups had significantly improved their average FMA, MI and FTHUE scores, with the average FMA score of group B significantly better than those of groups A and C. The average FTHUE score of group B was also significantly better than that of group A. Conclusions MT either alone or in combination with rTMS can improve cerebral motor cortex excitability and motor recovery after a stroke. Ten minute rTMS sessions followed by 50 min of MT have the best effect. Key words: Transcranial magnetic stimulation; Mirror therapy; Upper limb motor function; Stroke

Electroencephalogram-Electromyography Coupling Analysis in Stroke Based on Symbolic Transfer Entropy.

The coupling strength between electroencephalogram (EEG) and electromyography (EMG) signals during motion control reflects the interaction between the cerebral motor cortex and muscles. Therefore, neuromuscular coupling characterization is instructive in assessing motor function. In this study, to overcome the limitation of losing the characteristics of signals in conventional time series symbolization methods, a variable scale symbolic transfer entropy (VS-STE) analysis approach was proposed for corticomuscular coupling evaluation. Post-stroke patients (n = 5) and healthy volunteers (n = 7) were recruited and participated in various tasks (left and right hand gripping, elbow bending). The proposed VS-STE was employed to evaluate the corticomuscular coupling strength between the EEG signal measured from the motor cortex and EMG signal measured from the upper limb in both the time-domain and frequency-domain. Results showed a greater strength of the bi-directional (EEG-to-EMG and EMG-to-EEG) VS-STE in post-stroke patients compared to healthy controls. In addition, the strongest EEG–EMG coupling strength was observed in the beta frequency band (15–35 Hz) during the upper limb movement. The predefined coupling strength of EMG-to-EEG in the affected side of the patient was larger than that of EEG-to-EMG. In conclusion, the results suggested that the corticomuscular coupling is bi-directional, and the proposed VS-STE can be used to quantitatively characterize the non-linear synchronization characteristics and information interaction between the primary motor cortex and muscles.

Contralateral cortico-ponto-cerebellar pathways reconstruction in humans in vivo: implications for reciprocal cerebro-cerebellar structural connectivity in motor and non-motor areas

Cerebellar involvement in cognition, as well as in sensorimotor control, is increasingly recognized and is thought to depend on connections with the cerebral cortex. Anatomical investigations in animals and post-mortem humans have established that cerebro-cerebellar connections are contralateral to each other and include the cerebello-thalamo-cortical (CTC) and cortico-ponto-cerebellar (CPC) pathways. CTC and CPC characterization in humans in vivo is still challenging. Here advanced tractography was combined with quantitative indices to compare CPC to CTC pathways in healthy subjects. Differently to previous studies, our findings reveal that cerebellar cognitive areas are reached by the largest proportion of the reconstructed CPC, supporting the hypothesis that a CTC-CPC loop provides a substrate for cerebro-cerebellar communication during cognitive processing. Amongst the cerebral areas identified using in vivo tractography, in addition to the cerebral motor cortex, major portions of CPC streamlines leave the prefrontal and temporal cortices. These findings are useful since provide MRI-based indications of possible subtending connectivity and, if confirmed, they are going to be a milestone for instructing computational models of brain function. These results, together with further multi-modal investigations, are warranted to provide important cues on how the cerebro-cerebellar loops operate and on how pathologies involving cerebro-cerebellar connectivity are generated.

128 The Importance of Somatotopy to Achieve Clinical Benefit in Motor Cortex Stimulation for Pain Relief

Abstract INTRODUCTION The aim of this study was to search the relationship between the anatomical location and the eventual analgesic effect of each contact. METHODS 22 patients (14 men and 8 women) suffering from central and/or peripheral neuropathic pain were implanted with stimulation of the precentral cortex. The implantation of the electrodes was performed using intraoperative: 1) Anatomical identification by Neuronavigation with 3D MRI, 2) Somesthetic evoqued potentials monitoring to check the potential reverse over the central sulcus, 3) Electrical stimulations through the dura to identify the motor responses and its somatotopy. In order to locate postoperatively the electrodes, a 3D-CT was performed in each case and fused with the preoperative MRI. The clinical analgesic effects of cortical stimulation were collected on a regular basis (VAS reduction > 50%, drugs consumption). Data were analyzed to search a correlation between the anatomical position of contacts and analgesic effects. RESULTS >Post implantation analgesic effects were obtained in 18 (81.81%) patients out of 22. The analgesic effect was companied with reduction of the drugs consumption in 15 patients (68.18%). The post-operative 3D CT analysis shows a correspondence between the effective contacts localization and the motor cerebral cortex somatotopy in the patients with post-operative good analgesic effects. No correspondence was found between the contacts localization and the motor cerebral cortex somatotopy in the 4 patients with no analgesic effects. In three out of these four patients, analgesic effects were obtained after a new surgery allowing a replacement of the electrode position over the motor cortex somatotopy corresponding to the painful area. CONCLUSION This study shows the correlation between position of the contact over the precentral cortex and the analgesia obtained when the somatotopy of the stimulated cortex correspond to the painful area.

Glutamate Neonatal Excitotoxicity Modifies VEGF-A, VEGF-B, VEGFR-1 and VEGFR-2 Protein Expression Profiles During Postnatal Development of the Cerebral Cortex and Hippocampus of Male Rats.

Vascular endothelial growth factor (VEGF) exerts both neuroprotective and proinflammatory effects in the brain, depending on the VEGF (A-E) and VEGF receptor (VEGFR1-3) types involved. Neonatal monosodium glutamate (MSG) treatment triggers an excitotoxic degenerative process associated with several neuropathological conditions, and VEGF messenger RNA (mRNA) expression is increased at postnatal day (PD) 14 in rat hippocampus (Hp) following the treatment. The aim of this work was to establish the changes in immunoreactivity to VEGF-A, VEGF-B, VEGFR-1 and VEGFR-2 proteins induced by neonatal MSG treatment (4g/kg, subcutaneous, at PD1, 3, 5 and 7) in the cerebral motor cortex (CMC) and Hp. Samples collected from PD2 to PD60 from control and MSG-treated male Wistar rats were assessed by western blotting for each protein. Considering that immunoreactivity measured by western blotting is related to the protein expression level, we found that each protein in each cerebral region has a specific expression profile throughout the studied ages, and all profiles were differentially modified by MSG. Specifically, neonatal MSG treatment significantly increased the immunoreactivity to the following: (1) VEGF-A at PD8-PD10 in the CMC and at PD6-PD8 in the Hp; (2) VEGF-B at PD2, PD6 and PD10 in the CMC and at PD8-PD9 in the Hp; and (3) VEGFR-2 at PD6-PD8 in the CMC and at PD21-PD60 in the Hp. Also, MSG significantly reduced the immunoreactivity to the following: (1) VEGF-B at PD8-PD9 and PD45-PD60 in the CMC; and (2) VEGFR-1 at PD4-PD6 and PD14-PD21 in the CMC and at PD4, PD9-PD10 and PD60 in the Hp. Our results indicate that VEGF-mediated signalling is involved in the excitotoxic process triggered by neonatal MSG treatment and should be further characterized.

Cholinergic neurotransmission and olfactory function in obstructive sleep apnea syndrome: a TMS study

Background/objectiveOdor identification and discrimination are reduced in subjects with obstructive sleep apnea syndrome (OSAS), but the pathophysiology of the olfactory dysfunction in OSAS is still poorly understood. Experimental evidence suggests that olfactory impairment could be related to central cholinergic dysfunction. Short latency afferent inhibition (SAI) is a paired-pulse transcranial magnetic stimulation (TMS) protocol that gives the opportunity to test an inhibitory cholinergic circuit in the human cerebral motor cortex. The objective of the study was to assess the cholinergic function, as measured by SAI, in OSAS patients with olfactory impairment. MethodsWe applied SAI technique in 20 patients with OSAS and in 20 healthy control subjects; SAI values were correlated with the Sniffin' Sticks olfactory test results. ResultsSAI was reduced in OSAS patients when compared with control subjects. We also found a strong negative correlation between olfactory parameters and SAI. ConclusionsThese findings suggest that cholinergic dysfunction is a robust determinant of hyposmia also in OSAS patients. Reduced SAI values and presence of olfactory impairment might indicate an increased risk of cognitive decline in patients with OSAS.

Impaired cholinergic transmission in patients with Parkinson's disease and olfactory dysfunction

Olfactory dysfunction represents a frequent and disturbing non-motor manifestation of Parkinson's disease (PD). The pathophysiology of olfactory dysfunction in PD is still poorly understood. Experimental evidence suggests that olfactory impairment could be related to central cholinergic dysfunction. Short latency afferent inhibition (SAI) technique gives the opportunity to test an inhibitory cholinergic circuit in the human cerebral motor cortex. The objective of the study was to assess the cholinergic function, as measured by SAI, in PD patients with different degrees of olfactory dysfunction. We applied SAI technique in 31 patients with PD. These patients also underwent Olfactory Event-Related Potentials (OERPs) studies to objectively evaluate the olfactory system and a battery of neuropsychological tests to assess the cognitive functions. Absent OERPs indicated a severe olfactory dysfunction in 13 subjects. The presence of OERPs with an alteration in latency and/or amplitude can be considered as a borderline condition of slight alteration of smell and was found in other 15 patients. Only 3 patients showed normal OERPs. SAI was significantly reduced in the PD patients with absent OERPs compared with those with present but abnormal OERPs. Neuropsychological examination showed a mild cognitive impairment in 12 out of 13 PD patients with severe olfactory dysfunction, and in 3 out of the 15 patients with borderline olfactory dysfunction. SAI abnormalities and presence of severe olfactory impairment strongly support the hypothesis of cholinergic dysfunction in some patients with PD, who will probably develop a dementia. Longitudinal studies are required to verify whether SAI abnormalities in PD patients with olfactory dysfunction can predict a future severe cognitive decline.

Flow-metabolism uncoupling in the cervical spinal cord of ALS patients.

Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease. In ALS, both glucose consumption and neuronal intensity reportedly decrease in the cerebral motor cortex when measured by positron emission tomography (PET). In this study, we evaluated cervical spinal glucose metabolism, blood flow, and neuronal intensity of 10 ALS patients with upper extremity (U/E) atrophy both with 18F-2-fluoro-2-deoxy-D-glucose (18F-FDG) PET and 11C-flumazenil (11C-FMZ) PET. On the ipsilateral side of C5 and T1 levels, 18F-FDG uptake increased significantly (*p<0.05), and was correlated with the rate of progression of the ALS FRS-R-U/E score (R=0.645, *p=0.041). Despite this hyperglucose metabolism, the 11C-FMZ PET study did not show a coupled increase of spinal blood flow even though neuronal intensity did not decrease. These results indicate a strong correlation between hyperglucose metabolism and ALS progression alongside the uncoupling of flow-metabolism. This mechanism, which could result in subsequent motor neuronal death, may be a potential therapeutic target for ALS.

Contribution of TMS and rTMS in the Understanding of the Pathophysiology and in the Treatment of Dystonia.

Dystonias represent a heterogeneous group of movement disorders responsible for sustained muscle contraction, abnormal postures, and muscle twists. It can affect focal or segmental body parts or be generalized. Primary dystonia is the most common form of dystonia but it can also be secondary to metabolic or structural dysfunction, the consequence of a drug’s side-effect or of genetic origin. The pathophysiology is still not elucidated. Based on lesion studies, dystonia has been regarded as a pure motor dysfunction of the basal ganglia loop. However, basal ganglia lesions do not consistently produce dystonia and lesions outside basal ganglia can lead to dystonia; mild sensory abnormalities have been reported in the dystonic limb and imaging studies have shown involvement of multiple other brain regions including the cerebellum and the cerebral motor, premotor and sensorimotor cortices. Transcranial magnetic stimulation (TMS) is a non-invasive technique of brain stimulation with a magnetic field applied over the cortex allowing investigation of cortical excitability. Hyperexcitability of contralateral motor cortex has been suggested to be the trigger of focal dystonia. High or low frequency repetitive TMS (rTMS) can induce excitatory or inhibitory lasting effects beyond the time of stimulation and protocols have been developed having either a positive or a negative effect on cortical excitability and associated with prevention of cell death, γ-aminobutyric acid (GABA) interneurons mediated inhibition and brain-derived neurotrophic factor modulation. rTMS studies as a therapeutic strategy of dystonia have been conducted to modulate the cerebral areas involved in the disease. Especially, when applied on the contralateral (pre)-motor cortex or supplementary motor area of brains of small cohorts of dystonic patients, rTMS has shown a beneficial transient clinical effect in association with restrained motor cortex excitability. TMS is currently a valuable tool to improve our understanding of the pathophysiology of dystonia but large controlled studies using sham stimulation are still necessary to delineate the place of rTMS in the therapeutic strategy of dystonia. In this review, we will focus successively on the use of TMS as a tool to better understand pathophysiology, and the use of rTMS as a therapeutic strategy.

Somatotopic Representation of the Anterior Horn within Cervical Enlargement: Reappraisal of Known Doctrine Based on Clinicopathological Findings Seen in Hirayama Disease

Clinical features (weakness and amyotrophy of intrinsic hand muscles and obliquely distributed amyotrophy of forearm muscles, figure 1), needle electromyographic findings (distribution of neurogenic activities, figure 2), and pathological findings (ischemic necroses of the anterior horns between C6 and T1, figure 3) of Hirayama disease suggest that understanding of somatotopic representation of the anterior horn innervating arm muscles in the cervical enlargement of spinal cord differs from the known doctrine. Anterior horn cells of the intrinsic hand muscles are located between C7 and T1, those of forearm muscles and triceps brachii muscle as elbow extensor are, contrary to the known doctrine, located in C5 and C6, and those of elbow flexors such as biceps brachii and brachioradialis are located in C4 and above (figure 5). Development of dexterity in human hand may reflect development of cervical enlargement in accord with larger areas representing the hand and fingers on cerebral motor cortex.

Bilateral vocal cord paralysis with acute ischemic stroke

Vocal cords receive nerve supply from recurrent laryngeal nerve which is a branch of the vagus nerve. Cerebral motor cortex projects corticobulbar tracts to the motor nucleus (nucleus ambiguous) of the vagus found in medulla. Vagus nerve leaves the skull through jugular foramen and travels through the carotid sheath. The left vagus gives rise to left recurrent laryngeal nerve at the aortic arch, whereas the right vagus gives rise to right recurrent laryngeal nerve at the subclavian artery. Any disruption of this pathway by any entity will cause unilateral vocal cord paralysis. Strokes that affect the motor cortex do not cause unilateral vocal cord paralysis since vagus nerve nucleus receives corticobulbar tract from both sides of the brain. We present an unusual case of bilateral vocal cord paralysis caused by unilateral right insular stroke which is not related to this pathway.

Transcranial magnetic stimulation for monitoring the rehabilitation of upper-extremity function after stroke

Objective To evaluate the effect of the transcranial magnetic stimulation on upper-extremity function rehabilitation and changes in the excitability of cerebral cortex, and to evaluate from the viewpoint of electrophysiology the prognosis so as to guide the rehabilitation treatment of patients after stroke. Methods Forty-six patients in the early stage after a stroke were given TMS examinations of the ipsilateral brain region. Those with the motor evoked potentials (MEPs) amplitudes lower than 50 μV were classified into a motion-induced experimental negative group (the negative group), while those whose MEP amplitude reached 50 μV or more were classified as movement-induced positive (the positive group). Both groups were given the same treatment. Before and after 2, 4 and 8 weeks of treatment the Fugl-Meyer movement function rating scale was used to assess their bilateral upper limb movement function. TMS technology was used to detect any change in the resting motor threshold (RMT) and the amplitude (Amp) of MEPs in the motor cortex. The incubation period of the cortex (CL) and the central motor conduction time (CMCT) in the contralateral motor cerebral cortex were also observed. Results After 4 weeks of treatment, the average score of the positive group on Fugl-Meyer upper movement function rating scale reached (54.99±2.76), significantly higher than before treatment and significantly higher than the negative group's average (P 0.05). After the treatment the CL and CMCT had shortened significantly in the negative group compared to before the treatment (P 0.05). Conclusions The excitability of the contralateral motor cortex changes after a stroke. TMS can be used to characterize the MEP to monitor and predict recovery. This should help clinicians prepare more scientific rehabilitation plans. Key words: Transcranial magnetic stimulation; Stroke; Upper limb movement function; Cortical excitability

Knockdown of α-synuclein in cerebral cortex improves neural behavior associated with apoptotic inhibition and neurotrophin expression in spinal cord transected rats.

Spinal cord injury (SCI) often causes severe functional impairment with poor recovery. The treatment, however, is far from satisfaction, and the mechanisms remain unclear. By using proteomics and western blot, we found spinal cord transection (SCT) resulted in a significant down-regulation of α-synuclein (SNCA) in the motor cortex of SCT rats at 3days post-operation. In order to detect the role of SNCA, we used SNCA-ORF/shRNA lentivirus to upregulate or knockdown SNCA expression. In vivo, SNCA-shRNA lentivirus injection into the cerebral cortex motor area not only inhibited SNCA expression, but also significantly enhanced neurons' survival, and attenuated neuronal apoptosis, as well as promoted motor and sensory function recovery in hind limbs. While, overexpression SNCA exhibited the opposite effects. In vitro, cortical neurons transfected with SNCA-shRNA lentivirus gave rise to an optimal neuronal survival and neurite outgrowth, while it was accompanied by reverse efficiency in SNCA-ORF group. In molecular level, SNCA silence induced the upregulation of Bcl-2 and the downregulation of Bax, and the expression of NGF, BDNF and NT3 was substantially upregulated in cortical neurons. Together, endogenous SNCA play a crucial role in motor and sensory function regulation, in which, the underlying mechanism may be linked to the regulation of apoptosis associated with apoptotic gene (Bax, Bcl2) and neurotrophic factors expression (NGF, BDNF and NT3). These finds provide novel insights to understand the role of SNCA in cerebral cortex after SCT, and it may be as a novel treatment target for SCI repair in future clinic trials.

High-Resolution 7T MR Imaging of the Motor Cortex in Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis is a progressive motor neuron disorder that involves degeneration of both upper and lower motor neurons. In patients with amyotrophic lateral sclerosis, pathologic studies and ex vivo high-resolution MR imaging at ultra-high field strength revealed the co-localization of iron and activated microglia distributed in the deep layers of the primary motor cortex. The aims of the study were to measure the cortical thickness and evaluate the distribution of iron-related signal changes in the primary motor cortex of patients with amyotrophic lateral sclerosis as possible in vivo biomarkers of upper motor neuron impairment. Twenty-two patients with definite amyotrophic lateral sclerosis and 14 healthy subjects underwent a high-resolution 2D multiecho gradient-recalled sequence targeted on the primary motor cortex by using a 7T scanner. Image analysis consisted of the visual evaluation and quantitative measurement of signal intensity and cortical thickness of the primary motor cortex in patients and controls. Qualitative and quantitative MR imaging parameters were correlated with electrophysiologic and laboratory data and with clinical scores. Ultra-high field MR imaging revealed atrophy and signal hypointensity in the deep layers of the primary motor cortex of patients with amyotrophic lateral sclerosis with a diagnostic accuracy of 71%. Signal hypointensity of the deep layers of the primary motor cortex correlated with upper motor neuron impairment (r = -0.47; P < .001) and with disease progression rate (r = -0.60; P = .009). The combined high spatial resolution and sensitivity to paramagnetic substances of 7T MR imaging demonstrate in vivo signal changes of the cerebral motor cortex that resemble the distribution of activated microglia within the cortex of patients with amyotrophic lateral sclerosis. Cortical thinning and signal hypointensity of the deep layers of the primary motor cortex could constitute a marker of upper motor neuron impairment in patients with amyotrophic lateral sclerosis.

Nigella sativa oil alleviates ultrastructural alterations induced by tramadol in rat motor cerebral cortex

Tramadol is an opioid analgesic used to alleviate acute and chronic pain. Nigella sativa oil is one of the traditional remedies with antioxidant activity. This study was designed in order to investigate the ultrastructural alterations induced by tramadol in the rat cerebral cortex and to find out any possible protective effect of N. sativa oil against these alterations. Twenty-four male albino rats were assigned to three groups. Group I received intraperitoneal and oral normal saline for 30 days. Group II received intraperitoneal injections of tramadol 20mg/kg/day, 40mg/kg/day and 80mg/kg/day on the first, second and third 10 days of the study, respectively. Group III received intraperitoneal tramadol similar to Group II and oral N. sativa oil at a dose of 4ml/kg/day for 30 days. Specimens from the motor area were obtained and processed for transmission electron microscopy. In the tramadol-treated group, pyramidal and granular cells appeared shrunken and showed ultrastructural features of apoptosis such as nuclear membrane invaginations, chromatin margination, dilated rough endoplasmic reticulum, dilated Golgi saccules, and mitochondria with disintegrated cristae. The myelinated axons showed disorganization and splitting of the myelin sheath and contained vacuoles and abnormal mitochondria. Administration of N. sativa oil partially protected the cortical neurons and myelinated axons against tramadol-induced changes. In conclusion, N. sativa oil alleviates ultrastructural apoptotic changes induced by tramadol in the rat motor cerebral cortex.

Support vector machine and fuzzy C-mean clustering-based comparative evaluation of changes in motor cortex electroencephalogram under chronic alcoholism.

In this study, the magnitude and spatial distribution of frequency spectrum in the resting electroencephalogram (EEG) were examined to address the problem of detecting alcoholism in the cerebral motor cortex. The EEG signals were recorded from chronic alcoholic conditions (n=20) and the control group (n=20). Data were taken from motor cortex region and divided into five sub-bands (delta, theta, alpha, beta-1 and beta-2). Three methodologies were adopted for feature extraction: (1) absolute power, (2) relative power and (3) peak power frequency. The dimension of the extracted features is reduced by linear discrimination analysis and classified by support vector machine (SVM) and fuzzy C-mean clustering. The maximum classification accuracy (88%) with SVM clustering was achieved with the EEG spectral features with absolute power frequency on F4 channel. Among the bands, relatively higher classification accuracy was found over theta band and beta-2 band in most of the channels when computed with the EEG features of relative power. Electrodes wise CZ, C3 and P4 were having more alteration. Considering the good classification accuracy obtained by SVM with relative band power features in most of the EEG channels of motor cortex, it can be suggested that the noninvasive automated online diagnostic system for the chronic alcoholic condition can be developed with the help of EEG signals.

Agmatine Attenuates Brain Edema and Apoptotic Cell Death after Traumatic Brain Injury.

Traumatic brain injury (TBI) is associated with poor neurological outcome, including necrosis and brain edema. In this study, we investigated whether agmatine treatment reduces edema and apoptotic cell death after TBI. TBI was produced by cold injury to the cerebral primary motor cortex of rats. Agmatine was administered 30 min after injury and once daily until the end of the experiment. Animals were sacrificed for analysis at 1, 2, or 7 days after the injury. Various neurological analyses were performed to investigate disruption of the blood-brain barrier (BBB) and neurological dysfunction after TBI. To examine the extent of brain edema after TBI, the expression of aquaporins (AQPs), phosphorylation of mitogen-activated protein kinases (MAPKs), and nuclear translocation of nuclear factor-κB (NF-κB) were investigated. Our findings demonstrated that agmatine treatment significantly reduces brain edema after TBI by suppressing the expression of AQP1, 4, and 9. In addition, agmatine treatment significantly reduced apoptotic cell death by suppressing the phosphorylation of MAPKs and by increasing the nuclear translocation of NF-κB after TBI. These results suggest that agmatine treatment may have therapeutic potential for brain edema and neural cell death in various central nervous system diseases.

Effects of adjustment of transcranial direct current stimulation on motor function of the upper extremity in stroke patients

[Purpose] The purpose of this study was to examine the effects of transcranial direct current stimulation (tDCS) applied to the cerebral cortex motor area on the upper extremity functions of hemiplegic patients. [Subjects and Methods] Twenty four Patients with hemiplegia resulting from a stroke were divided into two groups: a tDCS group that received tDCS and physical therapy and a control group that received only physical therapy. A functional evaluation of the two groups was performed, and an electrophysiological evaluation was conducted before and after the experiment. Statistical analyses were performed to verify differences before and after the experiment. All statistical significance levels were set at 0.05. [Results] The results showed that functional evaluation scores for the elbow joint and hand increased after the treatment in both the experimental group and the control group, and the increases were statistically significantly different. [Conclusion] tDCS was effective in improving the upper extremity motor function of stroke patients. Additional research is warranted on the usefulness of tDCS in the rehabilitation of stroke patients in the clinical field.

Mossy fibers in the cerebellar hemisphere show delay activity in a delayed response task

To examine whether mossy fibers (MFs) in the cerebellar hemisphere show delay activity, we recorded MF activity during a wrist movement task with a random instructed delay period in two monkeys. Among 155 task-related MFs, 70 MFs (45%) demonstrated significant delay activity. Those MFs were widely distributed in the cerebellar hemisphere. Some of the activities were evoked by instruction cue presentation, whereas other activity started in anticipation of the upcoming go signal. For most MFs, the delay activities showed directional tuning. These patterns of the activity were in common with those of neurons in the cerebral motor cortices.