Motor Cortex Lesions Research Articles

Cerebrolysin Induces Motor Recovery Along with Plastic Changes in Motoneurons and an Increase in GAP43 Protein in the Ventral Spinal Cord Following a Kainic Acid Excitotoxic Lesion in the Rat Motor Cortex.

Lesions in the motor cortex induced by contusions or pathological insults can exert the degeneration of afferent neurons lying distal to these lesions. Axon degeneration and demyelination are hallmarks of several diseases sharing pathophysiological and clinical characteristics. These conditions are very disabling due to the disruption of motor abilities, with lesions that affect this area proving to be a therapeutic challenge, which has driven increasing efforts to search for treatments. Cerebrolysin (CBL) contains a mix of pig brain-derived peptides with activity similar to neurotrophic factors. Here, the effect of cerebrolysin administration on the motor impairment produced by kainic acid (KA) lesion of the motor cortex was evaluated in Sprague-Dawley female rats (n = 27), defining its effect on motoneurons dendritic tree changes, dendritic spine density and GAP43 presence in the ventral thoracolumbar regions of the spinal cord. Ten days after the KA lesion of the motor cortex, rats were administered cerebrolysin, and their motor performance was evaluated using the "Basso, Beattie, and Bresnahan" (BBB) and Bederson scores. Cerebrolysin administration improved motor activity according to the BBB and Bederson scales, along with increased dendritic intersections and dendritic spine density on motoneurons. There was also a significant increase in GAP43 protein, suggesting that CBL may promote plastic changes through this protein, among others. Hence, this study proposes that cerebrolysin could promote motor recovery following motor cortex lesions by driving neuronal changes and dendritic spine plasticity on motoneurons and an increase in GAP43 protein, along with other mechanisms.

Association between tumor location and toxicity outcomes after stereotactic radiosurgery for brain metastases.

Toxicities associated with stereotactic radiosurgery (SRS) are important when considering treatment and supportive management for patients with brain metastases. We herein assessed the association between brain metastasis location and risk of toxicity after SRS. We conducted a retrospective institutional review of patients treated with SRS for brain metastases between 2008 and 2023. Outcomes included radiation necrosis, seizure, local failure, and overall survival (OS). We reviewed 215 patients treated to 605 metastases (median diameter 10mm, IQR 5-17 mm), in the frontal (34%), cerebellar (19%), parietal (16%), temporal (13%), and occipital (13%) regions. Median follow-up was 16 months (IQR 7-36). New-onset seizures developed in 11% (19/174) of patients without prior seizure and was higher in patients with motor or sensory cortex lesions (12/48, 25%) on multivariate analysis (MVA, P = 0.02). SRS-related grade ≥ 2 symptomatic radionecrosis occurred in 6% (33/605) of lesions and correlated with larger metastasis volume (P < 0.001) and renal cell carcinoma histology (P < 0.05), while supratentorial location was nearly significant (MVA, P = 0.06). Median OS across all patients was 16 months (95% CI 12-20). Patients with symptomatic radiation necrosis had a longer median survival compared to those who did not (43 vs. 14 months, P = 0.002), which remained significant alongside Karnofsky performance status and extracranial disease on MVA. Brain metastasis location in the motor or sensory cortex is associated with increased risk of new-onset seizure following SRS and may warrant consideration of steroid and/or anti-epileptic prophylaxis. Symptomatic radiation necrosis is uncommon in the cerebellum and may be increasing with improvements in survival.

The corticospinal tract in multiple sclerosis: correlation between cortical excitability and magnetic resonance imaging measures.

Multiple sclerosis (MS) is a central nervous system disease involving gray and white matters. Transcranial magnetic stimulation (TMS) and magnetic resonance imaging (MRI) could help identify potential markers of disease evolution, disability, and treatment response. This work evaluates the relationship between intracortical inhibition and facilitation, motor cortex lesions, and corticospinal tract (CST) integrity. Consecutive adult patients with progressive MS were included. Sociodemographic and clinical data were collected. MRI was acquired to assess primary motor cortex lesions (double inversion and phase-sensitive inversion recovery) and CST integrity (diffusion tensor imaging). TMS outcomes were obtained: motor evoked potentials (MEP) latency, resting motor threshold, short-interval intracortical facilitation (ICF) and inhibition. Correlation analysis was performed. Twenty-five patients completed the study (13 females, age: 55.60 ± 11.49 years, Expanded Disability Status Score: 6.00 ± 1.25). Inverse correlations were found between ICF mean and each of CST radial diffusivity (RD) (ρ =-0.56; p < 0.01), CST apparent diffusion coefficient (ADC) (ρ=-0.44; p = 0.03), and disease duration (ρ=-0.46; p = 0.02). MEP latencies were directly correlated with disability scores (ρ = 0.55; p < 0.01). High ADC/RD and low ICF have been previously reported in patients with MS. While the former could reflect structural damage of the CST, the latter could hint towards an aberrant synaptic transmission as well as a depletion of facilitatory compensatory mechanisms that helps overcoming functional decline. The findings suggest concomitant structural and functional abnormalities at later disease stages that would be accompanied with a heightened disability. The results should be interpreted with caution mainly because of the small sample size that precludes further comparisons (e.g., treated vs. untreated patients, primary vs. secondary progressive MS). The role of these outcomes as potential MS biomarkers merit to be further explored.

Cortical drive may facilitate enhanced use of the paretic leg induced by random constraint force to the non-paretic leg during walking in chronic stroke.

The goal of this study was to determine the effects of applying random vs. constant constraint force to the non-paretic leg during walking on enhanced use of the paretic leg in individuals post-stroke, and examine the underlying brain mechanisms. Twelve individuals with chronic stroke were tested under two conditions while walking on a treadmill: random vs. constant magnitude of constraint force applied to the non-paretic leg during swing phase of gait using a custom designed robotic system. Leg kinematics, muscle activity of the paretic leg, and electroencephalography (EEG) were recorded during treadmill walking. Paretic step length and muscle activity of the paretic ankle plantarflexors significantly increased after walking with random and constant constraint forces. Cortico-cortical connectivity between motor cortices and cortico-muscular connectivity from the lesioned motor cortex to the paretic ankle plantarflexors significantly increased for the random force condition but not for the constant force condition. In addition, individuals post-stroke with greater baseline gait variability showed greater improvements in the paretic step length after walking with random force condition but not with the constant force condition. In conclusion, application of random constraint force to the non-paretic leg may enhance the use of the paretic leg during walking by facilitating cortical drive from the lesioned motor cortex to the paretic ankle plantarflexors. Results from this study may be used for the development of constraint induced locomotor intervention approaches aimed at improving locomotor function in individuals after stroke.

Motor cortex is responsible for motoric dynamics in striatum and the execution of both skilled and unskilled actions

Striatum and its predominant input, motor cortex, are responsible for the selection and performance of purposive movement, but how their interaction guides these processes is not understood. To establish its neural and behavioral contributions, we bilaterally lesioned motor cortex and recorded striatal activity and reaching performance daily, capturing the lesion's direct ramifications within hours of the intervention. We observed reaching impairment and an absence of striatal motoric activity following lesion of motor cortex, but not parietal cortex control lesions. Although some aspects of performance began to recover after 8-10days, striatal projection and interneuronal dynamics did not-eventually entering a non-motor encoding state that aligned with persisting kinematic control deficits. Lesioned mice also exhibited a profound inability to switch motor plans while locomoting, reminiscent of clinical freezing of gait (FOG). Our results demonstrate the necessity of motor cortex in generating trained and untrained actions as well as striatal motoric dynamics.

Self-organizing recruitment of compensatory areas maximizes residual motor performance post-stroke.

Whereas the orderly recruitment of compensatory motor cortical areas after stroke depends on the size of the motor cortex lesion affecting arm and hand movements, the mechanisms underlying this reorganization are unknown. Here, we hypothesized that the recruitment of compensatory areas results from the motor system's goal to optimize performance given the anatomical constraints before and after the lesion. This optimization is achieved through two complementary plastic processes: a homeostatic regulation process, which maximizes information transfer in sensory-motor networks, and a reinforcement learning process, which minimizes movement error and effort. To test this hypothesis, we developed a neuro-musculoskeletal model that controls a 7-muscle planar arm via a cortical network that includes a primary motor cortex and a premotor cortex that directly project to spinal motor neurons, and a contra-lesional primary motor cortex that projects to spinal motor neurons via the reticular formation. Synapses in the cortical areas are updated via reinforcement learning and the activity of spinal motor neurons is adjusted through homeostatic regulation. The model replicated neural, muscular, and behavioral outcomes in both non-lesioned and lesioned brains. With increasing lesion sizes, the model demonstrated systematic recruitment of the remaining primary motor cortex, premotor cortex, and contra-lesional cortex. The premotor cortex acted as a reserve area for fine motor control recovery, while the contra-lesional cortex helped avoid paralysis at the cost of poor joint control. Plasticity in spinal motor neurons enabled force generation after large cortical lesions despite weak corticospinal inputs. Compensatory activity in the premotor and contra-lesional motor cortex was more prominent in the early recovery period, gradually decreasing as the network minimized effort. Thus, the orderly recruitment of compensatory areas following strokes of varying sizes results from biologically plausible local plastic processes that maximize performance, whether the brain is intact or lesioned.

Local neuronal sleep after stroke: The role of cortical bistability in brain reorganization

BackgroundAcute cerebral ischemia triggers a number of cellular mechanisms not only leading to excitotoxic cell death but also to enhanced neuroplasticity, facilitating neuronal reorganization and functional recovery. ObjectiveTransferring these cellular mechanisms to neurophysiological correlates adaptable to patients is crucial to promote recovery post-stroke. The combination of TMS and EEG constitutes a promising readout of neuronal network activity in stroke patients. MethodsWe used the combination of TMS and EEG to investigate the development of local signal processing and global network alterations in 40 stroke patients with motor deficits alongside neural reorganization from the acute to the chronic phase. ResultsWe show that the TMS-EEG response reflects information about reorganization and signal alterations associated with persistent motor deficits throughout the entire post-stroke period. In the early post-stroke phase and in a subgroup of patients with severe motor deficits, TMS applied to the lesioned motor cortex evoked a sleep-like slow wave response associated with a cortical off-period, a manifestation of cortical bistability, as well as a rapid disruption of the TMS-induced formation of causal network effects. Mechanistically, these phenomena were linked to lesions affecting ascending activating brainstem fibers. Of note, slow waves invariably vanished in the chronic phase, but were highly indicative of a poor functional outcome. ConclusionIn summary, we found evidence that transient effects of sleep-like slow waves and cortical bistability within ipsilesional M1 resulting in excessive inhibition may interfere with functional reorganization, leading to a less favorable functional outcome post-stroke, pointing to a new therapeutic target to improve recovery of function.

Electrophysiological Changes on Laryngeal Motor Neuropathways Cause Voice Disorders for Postradiotherapy Patients with Nasopharyngeal Carcinoma

ObjectiveThis study explored electrophysiological changes in the laryngeal motor neuropathway and determined whether lesions in the laryngeal motor cortex (LMC) and its descending tract contribute to voice deterioration and peripheral nerve palsy in patients with nasopharyngeal carcinoma (NPC) post-radiotherapy (RT). Study DesignsProspective cohort study MethodsTwenty-two patients with NPC at 2 to 4 years post-RT (8 female and 14 male), 22 patients with NPC at 8 to 10 years post-RT (8 female and 14 male), and 22 healthy individuals (9 female and 13 male) were selected to test their magnetic evoked potentials (MEP), motor nerve conduction (MNC), and voice quality using transcranial magnetic stimulation (TMS), laryngeal electromyography (LEMG), and the XION DiVAS acoustic analysis software. Three groups were matched according to approximate age. Multiple comparisons were performed among the three groups. ResultsThe voice quality of post-RT patients with NPC deteriorated compared to that of healthy individuals. Bilateral LMC and their corticonuclear tracts to the bilateral ambiguous nuclei of post-RT patients with NPC were impaired according to multi-group comparisons of MEP amplitudes, latencies, and resting motor thresholds (RMT). The vagus and recurrent laryngeal nerves (RLN) of post-RT patients with NPC were impaired according to multi-group comparisons of the amplitude and latencies of the compound muscle action potential (CMAP) and latencies of f-waves. ConclusionsThe voice quality of patients with NPC deteriorated after RT. The pathogenesis of post-RT voice deterioration may involve radiation-induced injuries to the vagus, RLN, and bilateral LMC. Furthermore, radiation-induced injuries to the bilateral LMC may contribute to vagus and RLN palsies. These findings support the use of transcranial approaches to treating voice disorders and peripheral nerve palsies in post-RT patients with NPC.

Abstract TMP120: Contralesional Corticospinal Tract Reinnervates Cervical Spinal Anatomical Regions With Highest Pre-Lesion Synapse Density After Unilateral M1 Stroke in Mice

Introduction: Stroke leaves many patients with significant motor impairment. Following ischemic lesions of the rodent primary motor cortex, sprouting of the contralesional corticospinal tract (cCST) into the injured hemicord is associated with improved motor recovery. In adult mice, most corticospinal neurons project to spinal interneurons, and few synapse directly on alpha motor neurons. We examined the distribution of newly formed corticospinal synapses in the mouse spinal cord, using genetically encoded tracers, 3D microscopy, and a spinal atlas with machine learning-based automated classification and registration. Hypothesis: We tested the hypothesis that cCST neurons innervate homotopic regions in the injured hemicord after unilateral motor cortex stroke in adult mice. Method: We induced a photothrombotic motor cortex stroke or performed sham surgery (n=4 per group) in 8-11 week old male C57/B6 mice and administered a contralesional motor cortex injection of an anterograde adeno-associated virus expressing both membrane-targeted tdTomato and synaptically-targeted eGFP. Cervical spinal cords were subjected to volumetric imaging via serial two-photon tomography (TissueCyte 1000) to characterize synaptic and axonal density of cCST collaterals in whole cervical spinal cords in both stroke and sham mice. Unbiased, global quantification of axonal and synaptic density across the entire cervical cord was accomplished by the development of a custom automated image analysis pipeline, incorporating a novel 3D spinal cord reference volume, published spinal cord annotations comprising 47 distinct anatomical regions (SpinalJ), and machine learning based pixel classification. Results: We observed cCST synapses in the 6-week post-stroke injured hemicord innervating lamina IV &amp; IX most densely at C7 &amp; C8 (See Figure). Conclusions: Contralesional CST reinnervation of the denervated hemicord is targeted to both lamina and cervical level specific.

Endovascular Brain-Computer Interfaces in Poststroke Paralysis.

Stroke is a leading cause of paralysis, most frequently affecting the upper limbs and vocal folds. Despite recent advances in care, stroke recovery invariably reaches a plateau, after which there are permanent neurological impairments. Implantable brain-computer interface devices offer the potential to bypass permanent neurological lesions. They function by (1) recording neural activity, (2) decoding the neural signal occurring in response to volitional motor intentions, and (3) generating digital control signals that may be used to control external devices. While brain-computer interface technology has the potential to revolutionize neurological care, clinical translation has been limited. Endovascular arrays present a novel form of minimally invasive brain-computer interface devices that have been deployed in human subjects during early feasibility studies. This article provides an overview of endovascular brain-computer interface devices and critically evaluates the patient with stroke as an implant candidate. Future opportunities are mapped, along with the challenges arising when decoding neural activity following infarction. Limitations arise when considering intracerebral hemorrhage and motor cortex lesions; however, future directions are outlined that aim to address these challenges.

Measuring and Comparing Cortical Surface Area of Paracentral Lobule in a Tertiary care Hospital, Bangladesh

Background: The paracentral lobule is the area on medial surface of the cerebral cortex which extends from precentral sulcus to postcentral sulcus. Any trauma, tumor, or cerebral ischemia cause lesions of motor and sensory cortex of paracentral lobule. The result of this study is very important to the radiologists and neurosurgeons for diagnosis of above mentioned diseases and the practice of safe neurosurgery. This study was carried out to observe the cortical surface area of paracentral lobule in adult male and female Bangladeshi population,may help for future research. Methods: This cross- sectional study was conducted in the Department of Anatomy, Dhaka Medical College, Dhaka, during the period of January 2017 to December 2017. Total 70 adult Bangladeshi male &amp;female people were selected, among them 35 male and 35 female, age ranging from 20-65 years. CT scan image of brain in mid sagittal view was used for this study. Data were analyzed by Unpaired Student’s ‘t’ tests. Results: The surface area of motor cortex of right and left paracentral lobule was significantly higher (p&lt;0.01) in male.Surface area of sensory cortex of both paracentral lobule was significantly higher (p&lt;0.05) in male than female. Conclusion: The present study reveals significant difference in morphological measurements of right and left paracentral lobule between male and female of adult Bangladeshi population. Bangladesh J Medicine 2023; 34(3): 235-238

Фенотипи геміпарезу при різному ступені порушення кортико-спінальної іннервації

The impairment of motor functions after stroke has a polymorphic structure, in which a decrease in strength, impairment of selective control of movements, and the development of a spastic syndrome are most studied. With partial lesions of the primary motor cortex and impairment of corticospinal innervation, the recovery of motor control is supported by various processes of neuroplastic reorganization. Among humans, the influence of corticospinal innervation impairments on the functional state of motor control and the development of spasticity syndrome remains poorly understood. The aim of our work was to establish the phenotypes of the functional state of motor control with different severity of corticospinal innervation impairment among patients after an ischemic stroke. We found that when the corticospinal innervation is impaired on 32.9% [31.9-28.8] the control of the distal parts of the extremities and the synergies of the proximal parts are fractionated, and when on 92.9% [96-80.5] the control of the distal parts is lost and the number of synergies of proximal parts are decreases. With complete impairment of the corticospinal innervation, remains control of primitive synergies of only the proximal parts of the extremities. The development of spastic syndrome was higher in groups with increased segmental excitability, which was not directly related to the state of corticospinal innervation impairment. Thus, the phenotype of hemiparesis with an increase of the corticospinal innervation impairment is characterized by the dominance of a decrease of the strength of the distal parts of the extremities and an impairment of proximo-distal inter-joints coordination. Restoration of strength and control of the proximal parts of the extremities, axial muscles of the trunk and regulation of the muscles tone indicate the involvement of the alternative from the corticospinal, descending cortical and subcortical motor pathways.

Increased Risk of Aging-Related Neurodegenerative Disease after Traumatic Brain Injury.

Traumatic brain injury (TBI) survivors frequently suffer from chronically progressive complications, including significantly increased risk of developing aging-related neurodegenerative disease. As advances in neurocritical care increase the number of TBI survivors, the impact and awareness of this problem are growing. The mechanisms by which TBI increases the risk of developing aging-related neurodegenerative disease, however, are not completely understood. As a result, there are no protective treatments for patients. Here, we review the current literature surrounding the epidemiology and potential mechanistic relationships between brain injury and aging-related neurodegenerative disease. In addition to increasing the risk for developing all forms of dementia, the most prominent aging-related neurodegenerative conditions that are accelerated by TBI are amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), Parkinson's disease (PD), and Alzheimer's disease (AD), with ALS and FTD being the least well-established. Mechanistic links between TBI and all forms of dementia that are reviewed include oxidative stress, dysregulated proteostasis, and neuroinflammation. Disease-specific mechanistic links with TBI that are reviewed include TAR DNA binding protein 43 and motor cortex lesions in ALS and FTD; alpha-synuclein, dopaminergic cell death, and synergistic toxin exposure in PD; and brain insulin resistance, amyloid beta pathology, and tau pathology in AD. While compelling mechanistic links have been identified, significantly expanded investigation in the field is needed to develop therapies to protect TBI survivors from the increased risk of aging-related neurodegenerative disease.

State-dependent interhemispheric inhibition reveals individual differences in motor behavior in chronic stroke

ObjectiveTo investigate state-dependent interhemispheric inhibition (IHI) in chronic stroke survivors compared to neurotypical older adult controls, and test whether abnormal IHI modulation was associated with upper extremity motor behavior. MethodsDual-coil transcranial magnetic stimulation (TMS) measured IHI bi-directionally, between non-lesioned and lesioned motor cortex (M1) in two activity states: (1) at rest and (2) during contralateral isometric hand muscle contraction. IHI was tested by delivering a conditioning stimulus 8-msec or 50-msec prior to a test stimulus over contralateral M1. Paretic motor behavior was assessed by clinical measures of impairment, strength, and dexterity, and mirroring activity in the non-paretic hand. ResultsStroke survivors demonstrated reduced IHI at rest, and less IHI modulation (active – rest) compared to controls. Individual differences in IHI modulation were related to motor behavior differences where greater IHI modulation was associated with greater motor impairment and more mirroring. In contrast, there were no relationships between IHI at rest and motor behavior. ConclusionsAbnormal state-dependent interhemispheric circuit activity may be more sensitive to post-stroke motor deficits than when assessed in a single motor state. SignificanceCharacterizing state-dependent changes in neural circuitry may enhance models of stroke recovery and inform rehabilitation interventions.

Loss of Motor Cortical Inputs to the Red Nucleus after CNS Disorders in Nonhuman Primates.

The premotor (PM) and primary motor (M1) cortical areas broadcast voluntary motor commands through multiple neuronal pathways, including the corticorubral projection that reaches the red nucleus (RN). However, the respective contribution of M1 and PM to corticorubral projections as well as changes induced by motor disorders or injuries are not known in nonhuman primates. Here, we quantified the density and topography of axonal endings of the corticorubral pathway in RN in intact monkeys, as well as in monkeys subjected to either cervical spinal cord injury (SCI), Parkinson's disease (PD)-like symptoms or primary motor cortex injury (MCI). Twenty adult macaque monkeys of either sex were injected with the biotinylated dextran amine anterograde tracer either in PM or in M1. We developed a semiautomated algorithm to reliably detect and count axonal boutons within the magnocellular and parvocellular (pRN) subdivisions of RN. In intact monkeys, PM and M1 preferentially target the medial part of the ipsilateral pRN, reflecting its somatotopic organization. Projection of PM to the ipsilateral pRN is denser than that of M1, matching previous observations for the corticotectal, corticoreticular, and corticosubthalamic projections (Fregosi et al., 2018, 2019; Borgognon et al., 2020). In all three types of motor disorders, there was a uniform and strong decrease (near loss) of the corticorubral projections from PM and M1. The RN may contribute to functional recovery after SCI, PD, and MCI, by reducing direct cortical influence. This reduction possibly privileges direct access to the final output motor system, via emphasis on the direct corticospinal projection.SIGNIFICANCE STATEMENT We measured the corticorubral projection density arising from the PM or the M1 cortices in adult macaques. The premotor cortex sent denser corticorubral projections than the primary motor cortex, as previously observed for the corticotectal, corticoreticular, and corticosubthalamic projections. The premotor cortex may thus exert more influence than primary motor cortex onto subcortical structures. We next asked whether the corticorubral motor projections undergo lesion-dependent plasticity after either cervical spinal cord injury, Parkinson's disease-like symptoms, or primary motor cortex lesion. In all three types of pathology, there was a strong decrease of the corticorubral motor projection density, suggesting that the red nucleus may contribute to functional recovery after such motor system disorders based on a reduced direct cortical influence.

Beneficial Effects of Hyaluronan-Based Hydrogel Implantation after Cortical Traumatic Injury

Traumatic brain injury (TBI) causes cell death mainly in the cerebral cortex. We have previously reported that transplantation of embryonic cortical neurons immediately after cortical injury allows the anatomical reconstruction of injured pathways and that a delay between cortical injury and cell transplantation can partially improve transplantation efficiency. Biomaterials supporting repair processes in combination with cell transplantation are in development. Hyaluronic acid (HA) hydrogel has attracted increasing interest in the field of tissue engineering due to its attractive biological properties. However, before combining the cell with the HA hydrogel for transplantation, it is important to know the effects of the implanted hydrogel alone. Here, we investigated the therapeutic effect of HA on host tissue after a cortical trauma. For this, we implanted HA hydrogel into the lesioned motor cortex of adult mice immediately or one week after a lesion. Our results show the vascularization of the implanted hydrogel. At one month after HA implantation, we observed a reduction in the glial scar around the lesion and the presence of the newly generated oligodendrocytes, immature and mature neurons within the hydrogel. Implanted hydrogel provides favorable environments for the survival and maturation of the newly generated neurons. Collectively, these results suggest a beneficial effect of biomaterial after a cortical traumatic injury.

Modulation of Functional Connectivity in Response to Mirror Visual Feedback in Stroke Survivors: An MEG Study.

Background. Several brain regions are activated in response to mirror visual feedback (MVF). However, less is known about how these brain areas and their connectivity are modulated in stroke patients. This study aimed to explore the effects of MVF on brain functional connectivity in stroke patients. Materials and Methods. We enrolled 15 stroke patients who executed Bilateral-No mirror, Bilateral-Mirror, and Unilateral-Mirror conditions. The coherence values among five brain regions of interest in four different frequency bands were calculated from magnetoencephalographic signals. We examined the differences in functional connectivity of each two brain areas between the Bilateral-No mirror and Bilateral-Mirror conditions and between the Bilateral-Mirror and Unilateral-Mirror conditions. Results. The functional connectivity analyses revealed significantly stronger connectivity between the posterior cingulate cortex and primary motor cortex in the beta band (adjusted p = 0.04) and possibly stronger connectivity between the precuneus and primary visual cortex in the theta band (adjusted p = 0.08) in the Bilateral-Mirror condition than those in the Bilateral-No mirror condition. However, the comparisons between the Bilateral-Mirror and Unilateral-Mirror conditions revealed no significant differences in cortical coherence in all frequency bands. Conclusions. Providing MVF to stroke patients may modulate the lesioned primary motor cortex through visuospatial and attentional cortical networks.

Impact of cerebral palsy outline: A research review

Cerebral Palsy identifies a category of chronic movement and posture development disorders that involve impairment of activity, which are developed in the foetal or infant developing brain. It is understood that the possible causes of CP arise in the prenatal stage of development and the perinatal or natal phase, and the postnatal or post neonatal phase associated with congenital issues. It is the result of permanent static cerebral motor cortex lesion that occurs before or within 2 years of birth. While the lesion does not alter itself, the clinical symptoms shift as the child grows and develops. CP is the result of chronic static cerebral motor cortex lesion that occurs before or within two years of birth. Although the lesion does not alter itself, the clinical symptoms shift as the child grows and develops. The removal of spasticity helps many patients with CP to more easily and reliably use what selective motor ability they possess. CP associated spasticity can lead to complications of the musculoskeletal system such as contractures, pain, and subluxation. Related cognitive disorders result from the motor dysfunction.

Solitary cerebral metastasis from undiagnosed prostate cancer. Potential role of multiparametric MRI prostate in pre-treatment diagnostic protocols

A 73-year-old man presented with a three-week history of weakness and loss of co-ordination of the left-hand side and weakness of left-hand grip. MRI brain revealed an enhancing lesion in the right parietal lobe, adjacent to the central sulcus, with surrounding oedema and a small satellite lesion in motor cortex. Body CT and FDGPET CT revealed no obvious primary neoplasm. The patient underwent craniotomy with resection of the lesion, subsequent histopathology confirmed a metastatic carcinoma of likely prostate cancer primary origin. The patient was on 5-ARI (Finasteride) for lower urinary tract symptoms that decrease serum PSA levels to half and had benign feeling prostate on digital rectal examination (DRE). Subsequent MRI prostate confirmed presence of a lesion with very high probability of prostate cancer. The patient’s serum Prostate Specific Antigen (PSA) level was 6.8 (13.6 corrected for Finastride) which is relatively low in the context of metastatic disease. Given the recent NICE guidelines of using pre-biopsy multiparametric MRI (mpMRI) for diagnosis of prostate cancer, we suggest that in patients with cerebral metastases of unknown primary, with negative body CT, FDG PET-CT, low PSA and negative DRE, mpMRI prostate should be included in diagnostic protocol in the selected group of men, to enable early diagnosis and performing more suitable and targeted treatment. Keywords: Brain metastasis; prostate cancer; multiparametric MRI; metastasis of unknown origin

Immediate Effects of Anodal Transcranial Direct Current Stimulation on Postural Stability Using Computerized Dynamic Posturography in People With Chronic Post-stroke Hemiparesis

Postural stability is commonly decreased in individuals with chronic post-stroke hemiparesis due to multisystemic deficits. Transcranial direct current stimulation (tDCS) is a non-invasive method to modulate cortical excitability, inducing neuroplastic changes to the targeted cortical areas and has been suggested to potentially improve motor functions in individuals with neurological impairments. The purpose of this double-blinded, sham-controlled study was to examine the acute effects of anodal tDCS over the lesioned motor cortex leg area with concurrent limits of stability training on postural control in individuals with chronic post-stroke hemiparesis. Ten individuals with chronic post-stroke hemiparesis received either anodal or sham tDCS stimulation over the lesioned leg region of the motor cortex while undergoing 20 min of postural training. The type of stimulation to receive during the first session was pseudorandomized, and the two sessions were separated by 14 days. Before and immediately after 20 min of tDCS, the 10 m walk test, the Berg Balance Scale, and dynamic posturography assessments were performed. After a single session of anodal tDCS with concurrent postural training, we observed no changes in clinical measures of balance and walking, assessed using the Berg Balance Scale and 10 m walk test. For dynamic posturography assessments, participants demonstrated improvements in adaptation responses to toes-up and toes-down perturbations, regardless of the type of tDCS received. Additionally, improved performance in the shifting center of gravity was observed during anodal tDCS. Taken together, these preliminary findings suggest that tDCS can potentially be used as a feasible approach be incorporated into the rehabilitation of chronic post-stroke individuals with issues related to postural control and fear of falling, and that multiple sessions of tDCS stimulation may be needed to improve functional measures of postural control and walking.