Impaired Coordination Research Articles

O-07 RAPIDLY PROGRESSIVE LATE-ONSET X-LINKED ADRENOLEUKODYSTROPHY WITH A NOVEL MUTATION

Abstract Introduction X-linked adrenoleukodystrophy (X-ALD; OMIM:300100) is a progressive neurodegenerative disorder resulting from a congenital defect in the ABCD1 gene, which encodes the adrenoleukodystrophy protein (ALDP). Deficiency of ALDP leads to impaired peroxisomal β-oxidation of very long chain fatty acids (VLCFAs), causing their accumulation in the nervous system, testes, and adrenal cortex. Clinical Case A 20-year-old male patient was referred to the neurology clinic with a progressive speech disorder, impaired coordination while eating, incoherent speech, prolonged periods of dissociation, and cognitive disability for 6 months. Also clumsiness, unintentional falls, and involuntary arm movements were observed. In fact, when a more detailed history was obtained from the family, they mentioned that the patient had shown signs of clumsiness over the past three years. The patient was born healthy with no underlying health conditions, had an average academic record, and no history of illicit drug use. His neurologic examination did not reveal motor deficits, and the patient was attentive and oriented to person, place, time and situation. However, spasticity was observed in both lower extremities, and it was noted that the patient exhibited difficulty in following commands and doing some movements. His brain MRI revealed bilateral frontoparietal white matter patterns consistent with X-ALD. After that he was referred to our clinic. Adrenal insufficiency was detected, and he was started on hydrocortisone therapy. Elevated very long-chain fatty acid levels were also found. Genetic testing revealed a novel mutation (NM_000033.4 c.778dup p.(Ala260GlyfsTer41) in the ABCD1 gene, which was also detected in the patient’s female sibling. Subsequently, he developed gait disturbances, paraparesis, and sphincter dysfunction. The patient exhibited rapid progression and is currently bedridden, being fed through a percutaneous enteral gastrostomy (PEG) in a three months. According to the evaluation of the patient, it was determined that he was not suitable for gene therapy or stem cell transplant due to the high Loes score (19), rapid progression, and his age. Conclusion X-ALD is a rare disease with significant morbidity and a high mortality rate. Typically, affected boys present between four and eight years of age. Our case involves late-onset and rapid progression with a novel mutation.

Ataxia telangiectasia in a Bahraini child treated with intensive physiotherapy: A case report

Ataxia telangiectasia (AT) is a rare neurodegenerative condition with a prevalence of 1 in 40,000 to 1 in 300,000 worldwide. It involves a genetic mutation of chromosome 11q.26. The condition is inherited in an autosomal recessive manner causing atrophy of the cerebellum due to loss of Purkinje fibres. AT presents early in childhood and the clinical features depend on the type of mutation. The study is a case report of a rare genetic disorder of a 9-year-old female who came to the physiotherapy clinic with a diagnosis of AT. The patient was presented with progressively worsening gait problems with frequent falls, with complete dependence on assistance and impaired balance and coordination. The treatment program was 12 months divided into an intense physiotherapy program for two months followed by 10 months of two times per week of physiotherapy sessions. The program was divided into four elements which are: (1) Lifestyle changes, (2) Strengthening exercises, (3) Coordination exercises, and (4) Balance training exercises. The result showed a positive outcome in increasing the patient’s independence, increased muscle strength, reduced ataxia symptoms intensity, and the patient can carry out complex activities with the help of accessory orthosis devices.

Asymmetric projection of introspection reveals a behavioural and neural mechanism for interindividual social coordination

When we collaborate with others to tackle novel problems, we anticipate how they will perform their part of the task to coordinate behavior effectively. We might estimate how well someone else will perform by extrapolating from estimates of how well we ourselves would perform. This account predicts that our metacognitive model should make accurate predictions when projected onto people as good as, or worse than, us but not on those whose abilities exceed our own. We demonstrate just such a pattern and that it leads to worse coordination when working with people more skilled than ourselves. Metacognitive projection is associated with a specific activity pattern in anterior lateral prefrontal cortex (alPFC47). Manipulation of alPFC47 activity altered metacognitive projection and impaired interpersonal social coordination. By contrast, monitoring of other individuals’ observable performance and outcomes is associated with a distinct pattern of activity in the posterior temporal parietal junction (TPJp).

Taurine protection attenuates bisphenol-A-induced behavioral, neurochemical, and histopathological alterations in male rats.

Due to the continuous exposure to bisphenol-A (BPA), the current study was conducted to evaluate taurine's neuroprotective action against BPA's adverse effect on the brain. Rats were grouped into control, BPA-treated rats, and taurine + BPA-treated rats. At the end of the 35-day treatment period, the memory of the rats was evaluated using the novel object test and the Y-maze test. An open-field test was used to measure motor activity. The changes in monoamines, monoamine oxidase (MAO), acetylcholinesterase (AChE), Na+,K+,ATPase, oxidative stress, caspase-3, and histopathology were evaluated in the cortical and hippocampal tissues of all groups. Data analysis by ANOVA revealed that BPA treatment induced motor hyperactivity and short- and long-term memory impairment. In the cortex, BPA decreased serotonin (5-HT), norepinephrine (NE), MAO, Na+,K+,ATPase, and nitric oxide (NO) and increased dopamine (DA), AChE, lipid peroxidation (MDA), glutathione (GSH), and caspase-3. In the hippocampus, BPA increased 5-HT, DA, NE, MAO, AChE, MDA, NO, GSH, and caspase-3 and decreased Na+,K+,ATPase. These neurochemical changes were accompanied by significant histopathological alterations. Taurine treatment prevented memory impairment and motor hyperactivity induced by BPA. Taurine attenuated the neurochemical changes, oxidative stress, and caspase-3 level. Taurine improved the histopathological change induced by BPA. In conclusion, taurine significantly prevented BPA-induced cognitive deficits, motor coordination impairments, neurotransmitter imbalances, histopathological alterations, oxidative stress, and apoptosis.

Standardised activities in wheelchair rugby, comparison between athletes with coordination impairment and athletes with other impairments.

To determine if athletes with coordination impairment (CI) can continue playing wheelchair rugby (WR), while an evidence-based classification system, including impairment tests for CI is not yet available. This is a defensible practise if they show similar activity limitations as athletes with other eligible impairment types (OI) within the same sports class. Standardised activities were measured in 58 elite WR athletes; 14 with CI and 44 with OI. Wheelchair activities consisted of 20-meter sprint, 12-meter sprint with full stop, intermittent sprint (3-meter sprint, stop, 3-meter sprint, stop, 6-meter sprint with full stop), sprint-curve-slalom-curve, turn on the spot 180°, turn on the spot 90°, stop, turn 90°in the same direction, X-test (short circuit with sharp turns) without the ball. Ball activities consisted of maximal throwing distance, precision throwing short (25% of maximum throw) and long (75% of maximal throw) distance and X-test with the ball (pick-up the ball and dribble whilst pushing). Descriptive statistics were used and Spearman's Rank correlation was assessed for athletes with CI and OI for each outcome measure. Differences between athletes with CI and OI were assessed using a Mann-Whitney U test. Most activities showed a high correlation with the athlete class in both athletes with CI and athletes with OI. Furthermore, outcome measures of athletes with CI overlapped with athletes with OI in the same sports class for all activities. There was a trend for worse performance in athletes with CI in turn on the spot 90°, stop, turn 90°in the same direction, the short distance one handed precision throw (P 0.11)and in the X-test with the ball (P 0.10). Despite the current lack of evidence based impairment tests for CI, it is a defensible practise to not exclude athletes with CI from WR with the current classification system. The trends for differences in performance that were found can support athletes and coaches in optimising performance of athletes with CI.

Do not Forget to Measure the Head: Hydrocephalus Can Phenotypically Mimic Developmental Coordination Disorder.

Developmental Coordination Disorder (DCD) is a neurodevelopmental condition presenting with poor motor skill development and impaired coordination at a young age. To diagnose DCD, neurologic conditions explanatory for the phenotype, including structural brain abnormalities like hydrocephalus, must be first ruled out. However, these neurologic conditions may phenotypically mimic DCD, which can hamper their distinction. In this article, we report a patient in whom the initial diagnosis of DCD was withdrawn after the identification of acquired hydrocephalus. An important cue in this case was secondary macrocephaly (from +0.00 to +2.25 standard deviations over approximately 6 years' time). This case illustrates that, in children whose phenotypes seemingly fulfill the DCD criteria, it is important to rule out an underlying, treatable etiology before making the diagnosis of DCD. Since few structural brain abnormalities mimicking DCD may present with macrocephaly, including hydrocephalus, performing longitudinal head circumference measurements can be useful to timely identify these neurologic conditions.

Effectiveness of 'video-based interventions' of toothbrushing over other interventions on improvement of oral hygiene in children with Autism Spectrum Disorders (ASD): a systematic review and meta-analysis.

Children with Autism exhibit impairment of fine motor co-ordination and sensory sensibilities and hence can directly affect the toothbrushing leading to poor oral hygiene. This current systematic review and meta-analysis (SRMA) aims to evaluate the effectiveness of Video-based intervention of toothbrush training over other methods on improvement of oral hygiene in children with autism spectrum disorders (ASD) MATERIALS AND METHODS: Prospero no: (CRD42023450168). 'PubMed', 'Cochrane', 'Ovid' databases were searched from 1 January 1980 to 1 August 2023 using pre-defined search strategy. 212 titles were retrieved after, duplicate exclusion, removal of irrelevant titles led to the final inclusion of 13 articles for full text screening out of which 7 articles were included for the final analysis. Even though video intervention reported better outcomes in individual studies, pooled data showed no significant superiority over other interventions such as social stories and picture-based interventions in relation to toothbrushing in children with ASD as indicated by the Plaque Index score (PI-S) and Oral hygiene index score (OHI-S).

Evaluation of the Application of Clinical Practice Guideline Recommendations on the Classification of Patients With Neck Pain.

Background: Clinical practice guidelines (CPGs) are developed to synthesize evidence into recommendations for clinical practice. Minimal evidence exists on the evaluation practice of physical therapists in the treatment of patients with neck pain. Purpose: We sought to describe (1) the extent to which clinicians perform the Neck Pain CPG-recommended examination measures and (2) the percentage of patients properly classified. Methods: We retrospectively analyzed the electronic health records of 397 patients with neck pain at an ambulatory care setting in an academic medical center. The frequency of physical therapists' evaluation measures, subjective findings, positive examination results, and the percentage of patients properly classified into impairment-based categories (IBCs) were recorded. Descriptive statistics and χ2 tests were used to assess patient demographics and compare classification accuracy across IBCs. Results: Of the 397 patients, 56% were classified into an IBC. The most common IBC was neck pain with mobility deficits (24%), followed by neck pain with radiating pain (17%), neck pain with movement coordination impairments (NPMCIs) (8%), and neck pain with headache (6%). Neck pain with movement coordination impairment had the lowest percentage of proper classifications. Classification accuracy was highest when subjective and objective findings were combined and varied between IBCs. Conclusion: Our findings suggest that physical therapists evaluating patients with neck pain may have increased classification accuracy when subjective and objective findings are considered. Decreased classification accuracy was demonstrated in the NPMCI category, highlighting opportunities for further education and research.

Detection and severity classification of ataxia using gait features and a hybrid model

Ataxia, a neurological disorder characterized by impaired coordination and unsteady movements, presents significant challenges for accurate diagnosis and classification. traditional machine-learning (ML) and deep-learning (DL) models often struggle to achieve high accuracy in predicting and classifying this complex condition. This study addresses these limitations by introducing a novel hybrid model, XGBoost-multi-layer-perceptron (XGB-MLP), specifically designed to enhance the accuracy of ataxia prediction and classification. The objective of this research is to develop a more reliable and precise diagnostic tool that outperforms existing ML and DL approaches. The methodology involved integrating the strengths of XGBoost, known for its powerful gradient boosting, with the multi-layer perceptron (MLP) neural network, creating a robust hybrid model. The proposed XGB-MLP model was rigorously tested against conventional models like random forest (RF), logistic regression (LR), support vector machine (SVM), MLP, and standalone XGBoost. The findings reveal that the XGB-MLP model achieves outstanding accuracy rates of 98.91% for ataxia prediction and 97.91% for classification, significantly surpassing the performance of the traditional models.

Paraoxonase 1 ameliorates neurological symptoms and motor coordination impairment caused by cerebral ischemia-reperfusion injury.

The anti-atherosclerotic effects of high-density lipoprotein (HDL) prevent the onset of cerebral infarction and provide cerebroprotective effects against ischemia-reperfusion injury. These inhibitory effects have been attributed to its antioxidant, anti-inflammatory, and antithrombotic properties. However, pharmacotherapeutic strategies to clinically realize these effects have not been demonstrated. Therefore, we aimed to develop paraoxonase 1 (PON1), a hydrolytic enzyme associated with HDL that exhibits antioxidant and anti-inflammatory effects, as a novel therapeutic agent against ischemia-reperfusion injury in cerebral infarction. We established a method to extract PON1 from human plasma with high purity and recovery while maintaining its activity. The purified PON1 exhibited antioxidant activity against human-derived LDL and HDL. Furthermore, PON1 actively suppressed the oxidation chain reaction by hydrolyzing lipid peroxides. The HDL-binding ability of PON1 was evaluated based on its activity in fractionated HDL from mice administered PON1 intravenously, which showed that most intravenously administered PON1 specifically bound to HDL. The cerebroprotective effect of intravenously administered PON1 was assessed using a mouse middle cerebral artery ischemia-reperfusion model by measuring infarct volume, long-term neurological scores, and walking time on a rotarod. Administration of PON1 after reperfusion reduced infarct volume 24 h after ischemia-reperfusion. Additionally, daily administration of PON1 for three days significantly improved neurological scores and walking time by approximately one month. Analysis of gene arrays in brain tissue indicated that PON1 suppresses biological functions and pathways associated with oxidative stress, inflammation, vascular dysfunction, thrombosis, and fibrosis. PON1 enhances the cerebroprotective effects of HDL and is a potential candidate for acute stroke therapy.

Loss of PV Interneurons in the BLA May Contribute to Altered Network and Behavioral States in Chronically Epileptic Mice.

Psychiatric disorders, including anxiety and depression, are highly comorbid in people with epilepsy. However, the mechanisms mediating the shared pathophysiology are currently unknown. There is considerable evidence implicating the basolateral amygdala (BLA) in the network communication of anxiety and fear, a process demonstrated to involve parvalbumin-positive (PV) interneurons. The loss of PV interneurons has been well described in the hippocampus of chronically epileptic mice and in postmortem human tissue of patients with temporal lobe epilepsy (TLE). We hypothesize that a loss of PV interneurons in the BLA may contribute to comorbid mood disorders in epilepsy. To test this hypothesis, we employed a ventral intrahippocampal kainic acid model of TLE in mice, which exhibits profound behavioral deficits associated with chronic epilepsy. We demonstrate a loss of PV interneurons and dysfunction of the remaining PV interneurons in the BLA of chronically epileptic mice. Furthermore, we demonstrate altered principal neuron function and impaired coordination of BLA network and behavioral states in chronically epileptic mice. To determine whether the loss of PV interneurons contributes to these altered network and behavioral states, we partially ablated PV interneurons in the BLA by stereotaxically injecting AAV-Flex-DTA into the BLA of PV-Cre mice. Loss of PV interneurons in the BLA is sufficient to alter behavioral states, such as increasing avoidance behaviors and impairing fear learning. These data suggest that compromised inhibition in the BLA in chronically epileptic mice may contribute to behavioral deficits, suggesting a novel mechanism contributing to comorbid anxiety and epilepsy.

Study of the acute toxicity of an antibacterial agent for pigs and poultry based on amoxicillin on white rats

The article presents the results of a study of the acute toxicity of the veterinary drug “Amoksidev 60” in white rats. The drug “Amoksidev 60” is a powder for the preparation of an oral solution. 1 g of the drug contains the active ingredient: amoxicillin – 500 mg (as amoxicillin trihydrate – 573 mg); excipients: anhydrous citric acid – up to 1 g. The veterinary medicinal product is used to treat pigs, diseases of the digestive tract, and respiratory organs caused by microorganisms that are sensitive to amoxicillin. The acute toxicity of an antibacterial agent based on amoxicillin for pigs and poultry was studied. Safety at low doses: administration of the drug at a dose of 2000 mg/kg body weight did not cause clinical signs of acute poisoning, and no animal in this group died within 14 days. The median lethal dose (LD50) of the drug is 6899.69 ± 1119.51 mg/kg of body weight, which allows it to be classified as a practically non-toxic substance (V toxicity class). Clinical manifestations of intoxication: when the dose is increased to 7000–12000 mg/kg, pronounced symptoms of intoxication were observed, including impaired coordination, depression, clinical convulsions, and mortality, which increased depending on the dose. Hazard classification: by toxicity, it can be attributed to class V – practically non-toxic substances (LD50 5001–15000 mg/kg), and by the degree of danger to class IV – low-hazard substances (LD50 > 5000 mg/kg), which ensures the prospect of its use in veterinary practice, provided that the recommended dosages are observed. The study results of the acute toxicity of an antibacterial agent based on amoxicillin on white rats open new directions for further scientific Research. Further studies will be aimed at studying subchronic and chronic toxicity, namely, assessing the impact of long-term use of the drug on the physiological state and function of organs and systems of the body and identifying cumulative effects of the drug.

Impact of Contralateral Hemiplegia on Lower Limb Joint Kinematics and Dynamics: A Musculoskeletal Modeling Approach

This study investigates the biomechanical differences between typically developed (TD) individuals and those with contralateral hemiplegia (CH) using musculoskeletal modeling in OpenSim. Ten TD participants and ten CH patients were analyzed for joint angles and external joint moments around the three anatomical axes: frontal, sagittal, and transverse. The analysis focused on hip, pelvis, lumbar, knee, ankle, and subtalar joint movements, leveraging MRI-derived bone length data and gait analysis. Significant differences (p < 0.05) were observed in hip flexion, pelvis tilt, lumbar extension, and ankle joint angles, highlighting the impact of hemiplegia on these specific joints. However, parameters like hip adduction and rotation, knee moment, and subtalar joint dynamics did not show significant differences, with p > 0.05. The comparison of joint angle and joint moment correlations between TD and CH participants highlights diverse coordination patterns in CH. Joint angles show significant shifts, such as HF and LR (−0.35 to −0.97) and PR and LR (0.22 to −0.78), reflecting disrupted interactions, while others like HR and LR (0.42 to 0.75) exhibit stronger coupling in CH individuals. Joint moments remain mostly stable, with HF and HA (0.54 to 0.53) and PR and LR (−0.51 to −0.50) showing negligible changes. However, some moments, like KA and HF (0.11 to −0.13) and PT and KA (0.75 to 0.67), reveal weakened or altered relationships. These findings underscore biomechanical adaptations and compensatory strategies in CH patients, affecting joint coordination. Overall, CH individuals exhibit stronger negative correlations, reflecting impaired coordination. These findings provide insight into the musculoskeletal alterations in hemiplegic patients, potentially guiding the development of targeted rehabilitation strategies.

Intraventricular Administration of Exosomes from Patients with Amyotrophic Lateral Sclerosis Provokes Motor Neuron Disease in Mice.

Amyotrophic lateral sclerosis (ALS) is a severe disease of the central nervous system (CNS) characterized by motor neuron damage leading to death from respiratory failure. The neurodegenerative process in ALS is characterized by an accumulation of aberrant proteins (TDP-43, SOD1, etc.) in CNS cells. The trans-synaptic transmission of these proteins via exosomes may be one of the mechanisms through which the pathology progresses. The aim of this work was to study the effect of an intraventricular injection of exosomes obtained from the cerebrospinal fluid (CSF) of ALS patients on the motor activity and CNS pathomorphology of mice. The exosomes were obtained from two ALS patients and a healthy donor. Exosome suspensions at high and low concentrations were injected into the lateral brain ventricles of male BALB/c mice (n = 45). Motor activity and physiological parameters were evaluated twice a month; morphological examination of the spinal cord was performed 14 months after the start of the experiment. Nine months after administration of exosomes from the ALS patients, the animals started exhibiting a pathological motor phenotype; i.e., altered locomotion with paresis of hind limbs, coordination impairment, and increasing episodes of immobility. The motor symptoms accelerated after administration of a higher concentration of exosomes. The experimental group showed a significant decrease in motor neuron density in the ventral horns of the spinal cord, a significant increase in the number of microglial cells, and microglia activation. The TDP43 protein in the control animals was localized in the nuclei of motor neurons. TDP43 mislocation with its accumulation in the cytoplasm was observed in the experimental group. Thus, the triggering effect of the exosomal proteins derived from the CSF of ALS patients in the development of a motor neuron pathology in the experimental animals was established. This confirms the pathogenetic role of exosomes in neurodegenerative progression and makes it possible to identify a new target for ALS therapy.

Neural dynamics underlying coordination between training-induced habitual and goal-directed responses.

Understanding the neurocognitive mechanisms that govern the coordination of habitual and goal-directed behaviors is important, because impaired coordination will cause various behavioral disorders. However, inducing habitual responses in human beings through repetitive stimuli-response training in a laboratory setting is a challenge. Well-trained sports athletes, who have automatic perception-action associations toward expertise-related stimuli, provide a natural sample to address this critical knowledge gap. We recorded electroencephalograms (EEG) of well-trained sports athletes while they performed a Simon task with expertise-related stimuli. By manipulating the congruency between the location of expertise-related stimuli and the response hand, we dissociated automatic habitual response and goal-directed inhibition control. We observed a stronger behavioral congruency effect on expertise-related stimuli than neutral stimuli in sports athletes but not healthy controls. Furthermore, sports athletes exhibited larger response-locked lateralized readiness potentials and stronger frontocentral beta band (15-25Hz) activity in the congruent condition than the incongruent condition, which indicate an enhanced response tendency toward expertise-related stimuli. In contrast, prominent mid-frontal theta (3-7Hz) activity observed in the incongruent condition signaled the involvement of response inhibition. Additionally, lateralized readiness potentials amplitude and theta power showed significant correlation with performance efficiency. Taken together, these results suggest that sports athletes exhibit an enhanced coordination for expertise-related stimuli, involving automatic response preparation and proficient response inhibition through extensive training.

Genetic machinery which accompanies metaplasticity operates differentially in experimental model of autism.

The present study investigated metaplasticity-related mRNA expressions in valproic acid (VPA)-rats, focusing on the PI3K/AKT pathway. Wistar dams were treated with a single intraperitoneal injection of 600 mg/kg VPA or saline on embryonic day E12.5 or an equal volume of saline solution. Three behavioral tests were conducted on these males' offspring: grid-walking test, negative geotaxis test, and three-chamber social interaction test. Metaplasticity was induced in 60-day-old male progeny by giving high-frequency stimulation for 5minutes following low-frequency stimulation to the perforant pathway. For the baseline stimulation protocol (n= 6), stimulation was delivered to the dentate gyrus at the previously determined stimulation intensity (0.33 Hz 0.175 msec 30 s) for 75 min. The percent change of slope of field excitatory postsynaptic potential (fEPSP) and amplitude of population spike were calculated 55-60 min after induction protocol. The mRNA levels of PI3K, PTEN, AKT, GSK-3β, and MAPT were measured in the hippocampus by using quantitative rt-PCR. We found that offspring of VPA-treated rats showed significantly impaired sensorimotor coordination, decreased sociability, impaired preference for social novelty, and reduced input-output curve of fEPSP slope, compared to control animals. Despite a similar metaplastic response, mRNA levels of genes of interest were similar but considerably down-regulated after induction in offspring of VPA-treated dams. Our study provides evidence that the induced expression of autism-related genes has evolved to enable an adaptation mechanism during metaplastic control of long-term potentiation.

Brivaracitam Ameliorates Increased Inflammation, Oxidative Stress, and Acetylcholinesterase Activity in Ischemic Mice.

Cerebral ischemia is a medical condition that occurs due to poor supply of blood in the brain. Reperfusion being savage further exaggerates the tissue injury causing cerebral ischemia/reperfusion injury (CI/R). CI/R is marked by an impairment in release of neurotransmitter, excitotoxicity, oxidative stress, inflammation, and neuronal apoptosis. The current study has utilized brivaracetam (BRV), a synaptic vesicle protein 2A modulator in experimental model of CI/R injury. CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. Animals were assessed for learning and memory, motor coordination (Rota rod, lateral push, and inclined beam walking test), cerebral infarction, and histopathological alterations. Biochemical assessments were made for oxidative stress (thiobarbituric acid reactive species, reduced glutathione, catalase, superoxide dismutase), inflammation (tumor necrosis factor-α and interleukin-10), and acetylcholinesterase activity (AChE) in brain supernatants. CI/R animals showed impairment in learning, memory, and motor coordination, along with increase in cerebral infarction, and histopathological alterations. Furthermore, increase in brain oxidative stress, inflammation, and AChE activity were recorded in CI/R animals. Administration of BRV (10 mg/kg and 20 mg/kg; p.o.) was observed to recuperate CI/R induced impairments in behavioral, biochemical, and histopathological analysis. It may be concluded that BRV mediates neuroprotection during CI/R via decreasing brain oxidative stress, inflammation, and AChE activity.

Selective inhibition of T-type calcium channel preserves ischemic pre-conditioning mediated neuroprotection during cerebral ischemia reperfusion injury in diabetic mice.

Ischemic preconditioning (IPC) provides ischemic tolerance and neuroprotection during cerebral ischemia reperfusion (CI/R) injury. Diabetes abolishes the beneficial effects of conditioning phenomenon during CI/R. The study investigates the role of T-type calcium ion channel in IPC mediated protection during diabetes mellitus. The study employed Swiss Albino mice. Animals were divided into 3 normoglycaemic groups (Sham, CI/R, and IPC) and 4 hyperglycaemic groups (Sham, CI/R, IPC, and ML218 + IPC). CI/R injury was induced in Swiss Albino mice by occlusion of common carotid arteries followed by reperfusion. IPC was given prior to CI/R injury and diabetes was induced using streptozotocin (STZ). Animals were assessed for learning, memory, motor coordination, neurological function, cerebral infarction, edema, and histopathological alterations. Biochemical assessments were performed for calcium binding proteins (Calmodulin (CaM), calcium/calmodulin-dependent protein kinase II (CaMKII), and S100B), oxidative stress (4-hydroxy-2-nonenal (4-HNE)), glutathione (GSH), inflammation (nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), tumor necrosis factor (TNF-α), interleukin (IL-10)), inducible nitric oxide synthase (iNOS) levels, and acetylcholinesterase activity (AChE) in brain supernatants. NF-kB, iNOS, and S100B serum levels were also assessed. CI/R animals (normoglycemic and hyperglycaemic) showed impairment in learning, memory, motor coordination, and neurological function along with increase in cerebral infarction, edema, and histopathological alterations. Furthermore, increase in brain calcium-binding proteins, oxidative stress, inflammation, and AChE along with serum NF-kB, iNOS, and S100B levels were recorded in CI/R animals. IPC ameliorated CI/R induced behavioral, biochemical, and histopathological impairment, however no beneficial effects were observed in IPC (diabetic) mice. Administration of ML218 (10mg/kg; i.p.), a selective T-type calcium channel re-established the IPC mediated neuroprotection in CI/R diabetic animals. In conclusion, IPC-mediated neuroprotection was abolished in diabetic mice. T-type calcium ion channel antagonism plays an important role in the IPC-mediated neuroprotection during hyperglycaemia.

Capsaicin Protects Against Nigrostriatal Neurodegeneration Induced by Rotenone

Capsaicin, the principal pungent ingredient of hot pepper exerts neuroprotective effects. In this study, the effect of capsaicin on rotenone-induced Parkinson’s disease in mice was investigated. Mice were given subcutaneous rotenone injections (1.5 mg/kg, every other day) and at the same time treated with the vehicle, L-dopa (25 mg/kg) or capsaicin at doses of 0.5 or 1.0 mg/kg orally once a day for two weeks. Biochemical indices of oxidative stress, malondialdehyde, reduced glutathione and nitric oxide were determined in brain tissue and histopathological study of the brain was done. Behavioral tests included stair, wire hanging and wood walking tests. Results showed that rotenone treatment led to significant increases in brain malondialdehyde and nitric oxide contents parallel with marked depletion of reduced glutathione. Rotenone induced degeneration of pigmented neurons in substantia nigra and of cerebral cortex and hippocampus neurons. Rotenone impaired neuromuscular strength, motor balance and coordination. Treatment with capsaicin significantly ameliorated the neuronal degeneration caused by rotenone and improved motor function. Capsaicin alleviated the increase in lipid peroxidation (malondialdehyde) and nitric oxide and prevented the depletion of reduced glutathione in brain of rotenone-treated animals. These data indicate that capsaicin protects against rotenone-induced neuronal damage and this involves decreased level of oxidative stress. Capsaicin therefore might prevent cell death in the brain of Parkinson’s disease patients.

Effectiveness of Maximum Voluntary Contraction Using Surface Electromyography on Erector Spinae and Tensor Fascia Latae Muscle Along With Muscle Energy Technique in Chronic Non-Specific Low Back Pain

Background: Low Back Pain (LBP) one of the major health issues over the world. It affects quality of life and work absentness leads to disability. Non-specific Low Back Pain (NSLBP) does not have specified problem. In this type, muscle imbalance, distributed muscle strength, endurance, movement co-ordination impairment, poor posture might enhance the nociceptor stimuli.Muscle energy technique (MET) is an active manual technique focused over muscle stretching, strengthening, relaxing. Aims to restore normal joint mobility and reduce pain.Aim: To determine the effect of muscle energy technique in chronic non-specific low back pain.To study the effectiveness of muscle energy technique in subjects with chronic non-specific low back pain on pain, functional disability and Surface electromyography (SEMG) measures.Material and Method: A total of 40 subjects were included in the study. 20 subjects with CNSLBP were allocated in a group A. whereas group B was allocated with Core Muscle Strengthening exercises (CMSE) for three weeks. All the participants were clearly explained about the procedure and informed consent attained.In group A, MET was applied over four muscle groups namely quadratus Lumborum (QL), erector spinae (ES), iliopsoas, tensor fascia latae (TFL). SEMG study was done over the two muscles, ES and TFL. At rest period measurement was done after their maximum voluntary contraction was recorded. Results: Pre-post-test comparison was analysed by Wilcoxon’s matched pair test. Between group analysis done by Mann Whitney U test, the experimental groups exhibit VAS, ODI, SEMG-ES (Rt and Lt), TFL (t and Lt) shown significance at p value = 0.001. Conclusion: MET was effectively reducing functional disability, decreases pain, muscle strength improved in ES and TFL muscles of both sides evaluated through SEMG.