Decreased Motor Function Research Articles

Hubungan Tingkat Activity Daily Living dengan Tingkat Depresi pada Pasien Stroke di RSUD Prof Dr Margono Soekarjo Purwokerto

Stroke is the largest cause of disability worldwide and is second to heart disease. Problems often faced by stroke patients include the inability to perform activity daily living (ADL) due to decreased motor function. This inability causes many stroke patients to experience depression. Knowing the relationship between the level of activity daily living with the level of depression in stroke patients at Prof. Dr. Margono Soekarjo Purwokerto Hospital. This study is an observational quantitative study, with a cross sectional approach. The sample used in the study was stroke patients who did inpatient Adenium Prof Dr Margono Soekarjo Purwokerto Hospital as many as 48 respondents who were taken using nonprobability sampling technique. Data collection was done using a questionnaire, then processed and analyzed using Fisher's Exact Test. The average age of respondents is 56-65 years or the late elderly category, the gender of most respondents was female (58.3%). The education level of most respondents is elementary education (43.8), while the most dominant disease history is respondents who have a history of disease (60.4%). The ADL level of stroke patients in the Adenium room of Prof. Dr. Margono Soekardjo Purwokerto Hospital was mostly in the severe category (52.1%). The level of depression in stroke patients in the Adenium room of Prof. Dr. Margono Soekardjo Purwokerto Hospital mostly had depression in the mild category (45.8%). There is a relationship between the level of ADL with depression in stroke patients in the Adenium room of Prof. Dr. Margono Soekarjo Purwokerto Hospital.

Do toenail manganese and iron levels reflect brain metal levels or brain metabolism in welders?

Inhalation of welding fumes can cause metal accumulation in the brain, leading to Parkinsonian-like symptoms. Metal accumulation and altered neurochemical profiles have been observed using magnetic resonance imaging (MRI) in highly exposed welders, being associated with decreased motor function and cognition. While MRI is impractical to use as a health risk assessment tool in occupational settings, toenail metal levels are easier to assess and have been demonstrated to reflect an exposure window of 7–12 months in the past. Yet, it is unclear whether toenail metal levels are associated with brain metal levels or changes in metabolism, which are the root of potential health concerns. This study investigates whether toenail manganese (Mn) and iron (Fe) levels, assessed at several time points, correlate with brain Mn and Fe levels, measured by MRI, as well as brain GABA, glutamate (Glu), and glutathione (GSH) levels, measured by Magnetic Resonance Spectroscopy (MRS), in seventeen Mn-exposed welders. Quantitative T1 and R2* MRI maps of the whole brain, along with GABA, Glu, and GSH MRS measurements from the thalamus and cerebellum were acquired at baseline (T0). Toenail clippings were collected at T0 and every three months after the MRI for a year to account for different exposure periods being reflected by toenail clippings and MRI. Spearman correlations of toenail metal levels were run against brain metal and metabolite levels, but no significant associations were found for Mn at any timepoint. Cerebellar GSH positively correlated with toenail Fe clipped twelve months after the MRI (p = 0.05), suggesting an association with Fe exposure at the time of the MRI. Neither thalamic GABA nor Glu correlated with toenail Fe levels. In conclusion, this study cannot support toenail Mn as a proxy for brain Mn levels or metabolic changes, while toenail Fe appears linked to brain metabolic alterations, underscoring the importance of considering other metals, including Fe, in studying Mn neurotoxicity.

Mirogabalin inhibits scratching behavior of spontaneous model mouse of atopic dermatitis.

Introduction: Atopic dermatitis (AD) is one of the most prevalent intractable chronic itch diseases worldwide. In recent years, new molecular-targeted drugs have emerged, but side effects and economic challenges remain. Therefore, since it is important for AD patients to have a wider range of treatment options, it is important to explore new therapeutic agents. Gabapentinoids, gabapentin and pregabalin, have been shown to be effective for the clinical treatment of several chronic itch. Recently, mirogabalin (MGB) was developed as a novel gabapentinoid. MGB is a drug for neuropathic pain and has a margin of safety between its side effects and the analgesic effect for animal experiments. Herein, we showed that MGB exhibited an antipruritic effect in a mouse model of AD using NC/Nga mice. Methods and results: The oral administration of MGB (10mg/kg) inhibited spontaneous scratching behavior in AD mice and its effect was dose dependently. Then, when MGB (10mg/kg) was orally administrated to healthy mice, it did not affect motor function, including locomotor activity, wheel activity, and coordinated movement. Moreover, gabapentin (100mg/kg) and pregabalin (30mg/kg), inhibited spontaneous scratching behavior in AD mice and decreased motor function in healthy mice. Furthermore, intracisternal injection of MGB (10μg/site) significantly suppressed spontaneous scratching behavior in AD mice. Discussion: In summary, our results suggest that MGB exerts an antipruritic effect via the spinal dorsal horn using NC/Nga mice. We hope that MGB is a candidate for a novel therapeutic agent for AD with relatively few side effects.

Cognitive impairment and hippocampal neuronal damage in β-thalassaemia mice

β-Thalassaemia is one of the most common genetic diseases worldwide. During the past few decades, life expectancy of patients has increased significantly owing to advance in medical treatments. Cognitive impairment, once has been neglected, has gradually become more documented. Cognitive impairment in β-thalassaemia patients is associated with natural history of the disease and socioeconomic factors. Herein, to determined effect of β-thalassaemia intrinsic factors, 22-month-old β-thalassaemia mouse was used as a model to assess cognitive impairment and to investigate any aberrant brain pathology in β-thalassaemia. Open field test showed that β-thalassaemia mice had decreased motor function. However, no difference of neuronal degeneration in primary motor cortex, layer 2/3 area was found. Interestingly, impaired learning and memory function accessed by a Morris water maze test was observed and correlated with a reduced number of living pyramidal neurons in hippocampus at the CA3 region in β-thalassaemia mice. Cognitive impairment in β-thalassaemia mice was significantly correlated with several intrinsic β-thalassaemic factors including iron overload, anaemia, damaged red blood cells (RBCs), phosphatidylserine (PS)-exposed RBC large extracellular vesicles (EVs) and PS-exposed medium EVs. This highlights the importance of blood transfusion and iron chelation in β-thalassaemia patients. In addition, to improve patients’ quality of life, assessment of cognitive functions should become part of routine follow-up.

Abstract TMP118: Aged Maternal Gut Microbiome Impairs Offspring Behavior and Exacerbates Stroke Outcome

The microbiome plays a significant role in influencing general health. A disruption of the gut biome homeostasis, dysbiosis, can be both the effect of disease or a precondition. The maternal biome has been shown to play a vital role in offspring brain and immune development by shaping the metabolic environment for the embryo. Therefore, an aged dysbiotic maternal biome may increase stroke risk factors among offspring and additionally, worsen stroke outcome. Young female C57B6 mice 3-month (M) of age had their host gut bacteria cleared via antibiotic treatment prior to recolonization via fecal microbiome transplants from 3M control, and 14M middle aged female mice. After breeding, the subsequent offspring was aged to 14 months, followed by behavioral tests, glucose tolerance, prior to a transient 60-minute middle cerebral artery occlusion (MCAO or sham surgery). The maternal biome had a significant effect on offspring biome at 2M, 6M and 9M of age, shifting the beta-diversity of females significantly (p=<0.01), and males to a lesser extent (p=0.241), extending into adulthood. Additional sex specific changes were observed in adult mouse behavior with decreased motor function and increased anxiety being prevalent in male offspring at 2 months of age (p=0.0338 and 0.0261 respectively) but not in females. At 6 months of age female offspring from dysbiotic mothers exhibited significantly impaired object recognition abilities compared to control (p=>0.01). Once the offspring had been subjected to a 60 min MCAO, a spontaneous recovery was observed in NDS scores in all females and in the control males, but not in males from dysbiotic mothers, suggesting that male stroke outcome is negatively affected by dysbiotic mothers. The maternal microbiome has a significant impact on offspring biome composition and health. Mice from mothers with aged microbiome exhibited sex specific early life motor function and cognitive impairment. Additionally, male offspring from dysbiotic mothers have a worsened stroke outcome.

Changes in Resting-State Networks in Children with Growth Hormone Deficiency.

Purpose: Growth hormone deficiency (GHD) refers to the partial or complete lack of growth hormone. Short stature and slow growth are characteristic of patients with GHD. Previous neuroimaging studies have suggested that GHD may cause cognitive and behavioral impairments in patients. Resting-state networks (RSNs) are regions of the brain that exhibit synchronous activity and are closely related to our cognition and behavior. Therefore, the purpose of the current study was to explore cognitive and behavioral abnormalities in children with GHD by investigating changes in RSNs. Methods: Resting-state functional magnetic resonance imaging (rs-fMRI) data of 26 children with GHD and 15 healthy controls (HCs) were obtained. Independent component analysis was used to identify seven RSNs from rs-fMRI data. Group differences in RSNs were estimated using two-sample t-tests. Correlation analysis was employed to investigate the associations among the areas of difference and clinical measures. Results: Compared with HCs, children with GHD had significant differences in the salience network (SN), default mode network (DMN), language network (LN), and sensorimotor network (SMN). Moreover, within the SN, the functional connectivity (FC) value of the right posterior supramarginal gyrus was negatively correlated with the adrenocorticotropic hormone and the FC value of the left anterior inferior parietal gyrus was positively correlated with insulin-like growth factor 1. Conclusions: These results suggest that alterations in RSNs may account for abnormal cognition and behavior in children with GHD, such as decreased motor function, language withdrawal, anxiety, and social anxiety. These findings provide neuroimaging support for uncovering the pathophysiological mechanisms of GHD in children. Impact statement Children with growth hormone deficiency (GHD) generally experience cognitive and behavioral abnormalities. However, there are few neuroimaging studies on children with GHD. Moreover, prior research has not investigated the aberrant brain function in patients with GHD from the perspective of brain functional networks. Therefore, this study employed the independent component analysis method to investigate alterations within seven commonly observed resting-state networks due to GHD. The results showed that children with GHD had significant differences in the salience network, default mode network, language network, and sensorimotor network. This provides neuroimaging support for revealing the pathophysiological mechanisms of GHD in children.

Emodin inhibits HDAC6 mediated NLRP3 signaling and relieves chronic inflammatory pain in mice.

Chronic pain reduces the quality of life and ability to function of individuals suffering from it, making it a common public health problem. Neuroinflammation which is mediated by the Nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation in the spinal cord participates and modulates chronic pain. A chronic inflammatory pain mouse model was created in the current study by intraplantar injection of complete Freund's adjuvant (CFA) into C57BL/6J left foot of mice. Following CFA injection, the mice had enhanced pain sensitivities, decreased motor function, increased spinal inflammation and activated spinal astrocytes. Emodin (10 mg/kg) was administered intraperitoneally into the mice for 3 days. As a result, there were fewer spontaneous flinches, higher mechanical threshold values and greater latency to fall. Additionally, in the spinal cord, emodin administration reduced leukocyte infiltration level, downregulated protein level of IL-1β, lowered histone deacetylase (HDAC)6 and NLRP3 inflammasome activity and suppressed astrocytic activation. Emodin also binds to HDAC6 via four electrovalent bonds. In summary, emodin treatment blocked the HDAC6/NLRP3 inflammasome signaling, suppresses spinal inflammation and alleviates chronic inflammatory pain.

Indolent T-cell lymphoma with pleural effusion and neurological signs in a cat: A case report.

This case report describes a 10-year-old castrated male Russian Blue cat who was referred to the hospital for respiratory distress and coughing. Tests for FeLV and FIV infection were negative. Pleural fluid was removed and subjected to cytological and lymphocyte clonality analysis. Thoracic radiography and ultrasonography confirmed atelectasis in some pulmonary lobes. The cat was diagnosed with stage III small- to medium-cell T cell lymphoma, and was treated with prednisolone (5 mg/head) and L-asparaginase (10000 units/m2). With this treatment, the pleural effusion gradually subsided and respiratory signs improved. However, the cat developed decreased motor function of the hindlimbs, forelimbs, and tongue, leading to the administration of 1-(2-Chloroethyl)3-cyclohexyl-1-nitrosourea (CCNU) (10mg/head or 38 mg/m2) for suspected central nervous system infiltration of lymphoma. Neurological signs dramatically improved within seven days, and CCNU (15mg/head or 54 mg/m2) was administered five more times until day 284, after which it was replaced with chlorambucil (2mg/head every four days). On day 393, weight loss and abdominal lymphadenopathy were observed, and CCNU (10mg/head) was administered again on the day 407 but was ineffective. Unfortunately, the cat eventually died on the day 466 with marked abdominal lymphadenopathy.

Review of Risk Factors Associated With Biomarkers for Alzheimer Disease.

BACKGROUND: Alzheimer disease (AD) is a neurodegenerative disease with no cure. The number of individuals living with AD doubles every 5 years. The current clinical practice relies on clinical history, mental status tests, cerebrum imaging, and physical and neurological examinations; however, recent advances in the field of biomarkers have provided clues for the early detection of AD. High levels of tau and low levels of amyloid-β (Aβ) in cerebrospinal fluid are well-known biomarkers for AD. METHODS: A database search of PubMed, Ovid MEDLINE, and CINAHL was conducted to identify relevant articles published within the last 5 years. The search was limited to articles concerning adults 65 years or older and published in the English language. Twelve articles were included in the review. RESULTS: Risk factors of sleep disruption, depression, and motor function are implicated. Cerebrospinal fluid parameters for biomarkers of tau and Aβ were universally lower among Blacks compared with Whites, raising concern that norm reference may not be accurate for all populations. Older adults are more at risk for AD. Results are inconclusive regarding whether depression is related to Aβ and tau pathology. CONCLUSION: Nurses should screen for sleep architecture, depression, and motor function in their patients and educate them on good sleep hygiene. Sleep studies should be advocated for people with suspected sleep apnea to mitigate the risk factor related to abnormal Aβ and tau pathology. Falls and decreased motor function require screening because they may be early indicators of abnormal biomarkers leading to AD.

Microplastic Exposure and the of Parkinson’s Disease

Microplastics (MPs) are small particles or fragments of plastic that have leaked into the environment and ecosystems in recent decades. Numerous animal studies have suggested that an organism’s exposure to microplastics may evoke responses from the body that are similar to the pathogenesis of human diseases. In particular, a collection of evidence has suggested that microplastics exposure may mimic Parkinson’s disease pathology (decreased dopaminergic neurons and interrupted motor function). Parkinson’s disease is an often progressive and fatal neurodegenerative disease that is defined by the degeneration of dopaminergic neurons in the brain; this degeneration leads to decreased motor function and abnormal motor movements. Studies have indicated that, upon entering the body, microplastics may trigger oxidative stress, organ inflammation, neurotoxicity, and transgenerational effects. Parkinson’s disease diagnoses are predicted to greatly increase in upcoming generations while microplastics continue to enter the environment at growing rates, inciting a point of concern for the human population and other organisms. In this review, the possible effects of organisms’ exposure to microplastics are explored through the review of animal studies and the comparison of these findings to the pathogenesis of Parkinson’s disease. By understanding the ways in which MPs affect the body and contribute to PD and other neurodegenerative disorders, the danger that MPs pose toward living organisms can be recognized, necessitate further research, and encourage preventative measures against the leakage of MPs into the environment.

Mechanism of skeletal muscle atrophy after spinal cord injury: A narrative review.

Spinal cord injury leads to loss of innervation of skeletal muscle, decreased motor function, and significantly reduced load on skeletal muscle, resulting in atrophy. Factors such as braking, hormone level fluctuation, inflammation, and oxidative stress damage accelerate skeletal muscle atrophy. The atrophy process can result in skeletal muscle cell apoptosis, protein degradation, fat deposition, and other pathophysiological changes. Skeletal muscle atrophy not only hinders the recovery of motor function but is also closely related to many systemic dysfunctions, affecting the prognosis of patients with spinal cord injury. Extensive research on the mechanism of skeletal muscle atrophy and intervention at the molecular level has shown that inflammation and oxidative stress injury are the main mechanisms of skeletal muscle atrophy after spinal cord injury and that multiple pathways are involved. These may become targets of future clinical intervention. However, most of the experimental studies are still at the basic research stage and still have some limitations in clinical application, and most of the clinical treatments are focused on rehabilitation training, so how to develop more efficient interventions in clinical treatment still needs to be further explored. Therefore, this review focuses mainly on the mechanisms of skeletal muscle atrophy after spinal cord injury and summarizes the cytokines and signaling pathways associated with skeletal muscle atrophy in recent studies, hoping to provide new therapeutic ideas for future clinical work.

Possibilities of using navigational transcranial magnetic stimulation as an element of radiotherapy preparation of patients with brain tumors: a pilot study

INTRODUCTION: Navigational transcranial magnetic stimulation (NTMs) is used in neurosurgical practice to identify functionally important motor areas of the brain for the purpose of safe resection of a tumor focus. At the same time, when planning radiation therapy (LT) and determining the amount of irradiation, until recently, functionally significant zones of topical representation of skeletal muscles in the cerebral cortex were not taken into account. This study evaluates the use of mapping motor areas of the cerebral cortex using NTMs when planning LT in patients with malignant gliomas affecting the motor cortex.OBJECTIVE: To evaluate the possibilities of navigational transcranial magnetic stimulation in the pre-radiation preparation of patients with brain tumors.MATERIALS AND METHODS: The study included 31 patients with gliomas of a high degree of malignancy who received radiation and/or chemoradiotherapy at the RSCRT from 2020 to 2022. The median follow-up was 12.1 months (3.0–24.5 months), while all patients were followed up to the control, 3-month follow-up period after the end of the course of radiation therapy, 23 patients showed up for control after 6 months (two patients died between 3-month and 6-month control).Statistics: analysis was performed using the Statistica 10.0 software (StatSoft, Inc., USA).RESULTS: Three out of 31 patients had improved motor function, while eight out of 31 patients had decreased motor function. Moreover, when comparing the preoperative condition with the condition during control examinations six months after radiation therapy, motor function improved in three patients, and decreased in eight. Maps of motor zones of NTMs overlapped PTV by 41.2%. The average dose of Dmean maps of NTMs was 42.3 Gy (3.7–61.1 Gy) and 37.0 Gy (3.6–55.8 Gy) with a limit of 45 Gy per motor zone. Thus, the average dose of Dmean according to the maps of the motor zones of NTMs was significantly reduced by 5.3±3.3 Gy (14.3%, p<0.05). The average dose of Dmean on NTMs cards was reduced by 4.6±3.5 Gy (12.8%, p<0.05) to 37.8 Gy. The average volume of NTMs cards receiving a dose equal to or greater than 45 Gy and 55 Gy can be significantly reduced by 11.3% and 8.4%, respectively, with dose restriction (p<0.001). Anatomical ORS (optic nerve chiasm and brain stem) were not affected in relation to the average dose of Dmean or the maximum dose with an increase in the dose to GTV.DISCUSSION: In our study, it was shown that maps of the motor zones of NTMs can be used in the planning of LT patients with gliomas of high malignancy. To date, the primary motor cortex has not been considered as an OR in such patients. The results of the study demonstrated that the dose in relation to the maps of the motor zones of NTMs can be significantly reduced without affecting the therapeutic doses for PTV.CONCLUSION: LT planning using NTMs motor maps can help reduce the radiation dose to the motor cortex in primary LT, although the motor cortex appears morphologically rather insensitive to LT compared to speech zones and areas of high-order cognitive processes, such as the temporal and limbic cortex.

Malnutrition in hospitalized cancer patients: A single-center, cross-sectional study in Southern Vietnam.

Malnutrition in cancer patients reduces response to chemotherapy, increases the hospitalization costs, hospital infections, and deaths. The aim of this study was to determine the prevalence, level of malnutrition, and its related factors in cancer patients at a local hospital in Southern Vietnam. A descriptive cross-sectional study was performed on all 118 cancer patients who were undergoing inpatient treatment at Long An General Hospital, Vietnam from May to September 2020. Data were collected from patients by face-to-face interviewing using a subjective global assessment (SGA) and from medical records. Malnutrition is divided into three groups: SGA-A (normal), SGA-B (mild/moderate/suspected malnutrition), SGA-C (severe malnutrition). Multivariable logistic regression is used to identify factors related to malnutrition with statistical significance p < 0.05. Out of 118 participants, 72 (61.0%) were males and 84 (71.2%) aged ⩾60 years. The prevalence of malnutrition in cancer patients was 84.7% (100/118), in which 33% (39/118) were severe (SGA-C) and 51.7% (61/118) were mild-moderate (SGA-B). Pancreatic and lung cancers are the most malnourished. The results of multivariate logistic regression analysis showed that the factors related to malnutrition in cancer patients were gastrointestinal symptoms lasting 2 weeks (odds ratio: 6.10, 95% confidence interval: 1.12-33.35), patients with decreased motor function (odds ratio: 13.73, 95% confidence interval: 2.56-73.86), blood albumin <35 g/l (odds ratio: 6.42, 95% confidence interval: 1.54-26.82), and blood lymphocyte ⩽ 1700 cells/mm3 (odds ratio: 5.36, 95% confidence interval: 1.31-21.97). There was a high proportion of malnutrition in cancer patients. Therefore, it is necessary to strengthen nutrition counseling and intervention for these patients, especially those that have prolonged gastrointestinal symptoms, reduced motor function, and low blood albumin or low blood lymphocytes.

Sex-specific associations between cord blood lead and neurodevelopment in early life: The mother-child cohort (Shanghai, China)

The extent to which neurodevelopment is affected by prenatal lead exposure has not been conclusive. In addition, studies on the effects of sex on these relationships are inconsistent. The aim of this study was to investigate the impact of cord blood lead on neurodevelopment in children within sex subgroups. A total of 275 mother-child pairs from the Shanghai mother-child cohort were included. Umbilical cord blood lead was measured using graphite furnace atomic absorption spectrophotometry. The Bayley Scales for Infant Development-III (BSID-III) was used to measure the neurodevelopment of infants at the age of 18 ± 1.5 months. The median and interquartile range of cord blood lead levels in the total participants, male, and female children were 44.0 (24.5) μg/L, 44.0 (24.3) μg/L, and 46.0 (24.0) μg/L, respectively. According to multiple linear regression, cord blood lead concentrations showed a negative association with fine motor scores in all models associated with female children (β = −1.5; 95%confidence interval: −2.6, −0.4). However, prenatal lead levels were not associated with any of the BSID-III scores in male children. In addition, cord serum DHA was found positively related to fine motor scores in male children. Our findings suggest that prenatal lead exposure could lead to decreased motor function, although this phenomenon was only observed in female children. And DHA may be a protective factor against lead exposure in boys. Thus, further studies are needed to investigate the associations between prenatal lead exposure and neurobehavioral development, as well as the mechanism of sex differences.

Natural Compounds That Enhance Motor Function in a Mouse Model of Muscle Fatigue.

Musculoskeletal disease can be a serious condition associated with aging that may lead to fractures and a bedridden state due to decreased motor function. In addition to exercise training to increase muscle mass, increasing muscle function with the intake of functional foods is an effective treatment strategy for musculoskeletal disease. Muscle-specific SOD2-deficient mice (muscle-Sod2-/-) show a severe disturbance in exercise in association with increased mitochondrial reactive oxygen species, as well as mitochondrial dysfunction and muscle damage. In the present study, to develop a therapeutic strategy for musculoskeletal disease, we searched for substances that enhanced motor function among functional compounds by in vivo screening using muscle-Sod2-/- mice as a muscle fatigue model. We administered 96 compounds, including antioxidants, to muscle-Sod2-/- mice and assessed their effects on treadmill performance. Among the administered compounds, gossypin, genistein, kaempferol, taxifolin, fumaric acid, β-hydroxy-β-methylbutyrate Ca, and astaxanthin, which are dietary functional food factors, increased forced running time in muscle-Sod2-/- mice. In addition, troglitazone, tempol, trolox, and MnTE-2-PyP, which are antioxidants, also significantly increased the running ability of muscle-Sod2-/- mice. These results suggest that the intake of functional foods with antioxidant activity can improve motor function. Muscle-Sod2-/- mice, as a muscle fatigue model, are suitable for the in vivo screening of functional substances that promote improvements in exercise and muscle performance.

SARC-F predicts poor motor function, quality of life, and prognosis in older patients with cardiovascular disease and cognitive impairment

ObjectivesWe investigated whether SARC-F scores were associated with motor function, quality of life (QOL) related to physical function, and prognosis in older patients with cardiovascular disease (CVD) and cognitive impairment. MethodsThis was a retrospective cross-sectional cohort study. The study population consisted of 408 patients with CVD (≥60 years old) who completed the SARC-F questionnaire and Mini-Cog, a cognitive function test, at discharge. Sarcopenia was defined as a total SARC-F score ≥ 4 points. Patients who were cognitively-preserved (Mini-Cog score ≥ 3 points) were excluded. Patients completed the handgrip strength, leg strength, usual gait speed, 6-minute walking distance, short physical performance battery score, and 36-item Short-Form Health Survey Physical Functioning (SF-36PF) tests before discharge. Associations of SARC-F with physical function, QOL, and prognoses (i.e., composite of all-cause death and emergency CVD rehospitalization and the number of CVD rehospitalizations) were investigated. ResultsSarcopenia (SARC-F score ≥ 4 points) was associated with poorer motor function test outcomes and SF-36PF scores (all P < 0.001). The correlations remained significant after adjusting for comorbidities (e.g., anemia, prior heart failure, and renal dysfunction). Sarcopenia was also associated with a poorer prognosis (hazard ratio: 1.574; 95 % confidence interval [CI], 1.011–2.445) and an increased risk of CVD rehospitalization (incidence rate ratio: 1.911; 95 % CI, 1.312–2.782) after adjusting for comorbidities. Conclusions and implicationsIn older patients with CVD and cognitive impairment, the SARC-F questionnaire may be a simple and inexpensive tool for identifying patients with decreased motor function and a poor prognosis.

Cluster Analysis of Biomechanical Gait Data and Pain Score as a Potential Classification of Severity in Knee Osteoarthritis

Osteoarthritis (OA) is the most common type of arthritis affecting approximately 240 million people globally, with increasing prevalence with age. The knee is the most prevalent joint affected by OA and it causes physical disability and decreased motor function which consequently affects the activity of daily living including mobility. Pain is the main symptom that is characterized in OA, which is measured using self-rated scales or questionnaires to determine several aspects of the pain including the intensity, frequency, and pattern. Quantifying pain is a standard clinical practice to diagnose and monitor symptomatic OA, however, its application for severity assessment is not well explored. To date, the severity assessment of knee OA is only by radiographic severity assessment that does not necessarily reflect the symptomatic OA. In this study, gait analysis was performed on symptomatic knee OA patients. Distinctive gait kinematic features were extracted using principal component analysis (PCA). Pain score and the gait features including spatiotemporal and kinematics were used for clustering analysis. Two clustering algorithms, K-means and K-medoids were conducted to cluster samples with similar features to assess knee OA characterization. The clustering solutions were evaluated based on three measures which are the Davies Bouldin index, Calinzki Harabasz index, and Silhouette index. This study discovered that majority of the datasets which is 5 out of 9 datasets had the best performance (fulfill at least 2 out of 3 performance index criteria) when the number of clusters, k is 4 and using the k-means algorithm. These clustering models can be used in the future as the labeling class of symptomatic knee OA that is based on pain and gait characteristics of knee OA. Future studies are suggested to test other pain assessment scores, include other gait features such as kinetic and muscle activity features, and employ various types of feature selection methods to improve the clustering performance.

A rare case of transverse myelitis in a patient with Lyme disease

Acute transverse myelitis (ATM) is an inflammatory disease of the spinal cord, characterized by rapid onset of bilateral neurological symptoms. The term myelitis refers to inflammation of the spinal cord, which often leads to demyelination. The clinical finding of a pattern of altered sensation is often a horizontal band-like sensation at the dermatomal level of the lesion, with sensory changes below. The symptoms usually develop over hours to days; they typically present as muscle weakness, ascending paralysis, and autonomic dysfunction. Recovery is variable, but often prolonged over many months, and can lead to a wide range of deficits.1 Our report reviews a unique case of transverse myelitis in a patient with Lyme disease. A 27 year old male presented to the emergency department with past medical history of diabetes mellitus and hyperlipidemia with a week long history of fever to 102℉, non-productive cough, nausea, and decreased motor function and sensation in the bilateral lower extremities. Strength was intact in bilateral biceps, triceps, and wrists, but diminished in bilateral hips, knees, and ankles. Sensation to light touch was diminished from the level of T8 and below, fine touch sensation diminished from the level of T10 and below, and there was diminished proprioception in bilateral toes. There was intact pain sensation in all extremities and hyperreflexia in bilateral upper extremities. An MRI was obtrained which demonstrated cervical syrinx with expansion of the spinal cord and resultant cervical stenosis with cord compression indicating need for surgical intervention. A posterior cervical decompressive laminectomy at levels C4-C7 and posterior thoracic decompressive laminectomy at level T1 were scheduled, with a subsequent lumbar puncture. Serum findings were significant for elevated Lyme disease antibody titer (7.89) and antibody reaction to 8 borrelial proteins. After detection of Lyme disease, the patient was started on antibiotics. Over the course of the hospital stay, motor function continually improved with the aid of physical therapy. Sensation also significantly improved. Lyme disease may not always be identifiable with CSF collection from lumbar puncture, and as a result the etiology of ATM may go unknown. Guillain-Barre syndrome is a common differential which has a similar presentation. However, the treatment consists of plasmapheresis and immunoglobulin. This is an important distinction in order to to provide the appropriate treatment modalities to the patient.

Neuroprotective effect of Geijigadaehwang-tang against trimethyltin-induced hippocampal neurodegeneration: An in vitro and in vivo study

Ethnopharmacological relevancePatients with dementia are diagnosed with deficiency patterns and interior patterns in traditional Chinese medicine due to decreased physical strength, mental atrophy including cognitive function, and decreased motor function in the gastrointestinal tract. Since “greater yin symptom” in Shanghanlun has been interpreted as interior, deficiency, and cold pattern in traditional Chinese medicine, it is necessary to determine whether Geijigadaehwang-tang (GDT) has therapeutic effects on neurodegenerative diseases and the underlying mechanism if it has such effects.Aims of the study: Trimethyltin (TMT), a neurotoxic organotin compound, has been used to induce several neurodegenerative diseases, including epilepsy and Alzheimer’s disease. This study aimed to evaluate the therapeutic efficacy of GDT for TMT-induced hippocampal neurodegeneration and seizures and to determine the mechanisms involved at the molecular level. Materials and methodsThe main components of GDT were analyzed using ultra-performance liquid chromatography. TMT was used to induce neurotoxicity in microglial BV-2 cells and C57BL6 mice. GDT was administered at various doses to determine its neuroprotective and seizure inhibition effects. The inhibitory effects of GDT on TMT-induced apoptosis, inflammatory pathways, and oxidative stress pathways were determined in the mouse hippocampal tissues. ResultsGDT contained emodin, chrysophanol, albiflorin, paeoniflorin, 6-gingerol, and liquiritin apioside. In microglial BV-2 cells treated with TMT, GDT showed dose-dependent neuroprotective effects. Oral administration of GDT five times for 2.5 days before and after TMT injection inhibited seizures at doses of 180 and 540 mg/kg and inhibited neuronal death in the hippocampus. In hippocampal tissues extracted from mice, GDT inhibited the protein expression of ionized calcium binding adaptor molecule 1, glial fibrillary acidic protein, nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing protein 3, and phosphorylated nuclear factor (NF)-κB/total-NFκB ratio. Additionally, GDT inhibited the messenger RNA levels of tumor necrosis factor-α, inducible nitric oxide synthase, apoptosis-associated speck-like protein containing a caspase recruitment domain, caspase-1, interleukin-1β, nuclear factor erythroid-2-related factor 2, and heme oxygenase-1. ConclusionThis study’s results imply that GDT might have neuroprotective potential in neurodegenerative diseases through neuronal death inhibition and anti-inflammatory and antioxidant mechanisms.

Olive Polyphenol as Neuroprotective in Chronic Cervical Myelopathy Rabbit Model

BACKGROUND: Olive polyphenols are known to be an anti-oxidants and anti-inflammatory agents. AIM: The purpose of this study was to determine the potential neuroprotective effect on chronic cervical myelopathy rabbit model. METHODS: This study was divided into six groups; control negative (Sham-Operated) group, control positive 1 and 2, treatment groups 1, 2, and 3. Olive leaf extract (OLE) gives 350 mg/kg BW and spinal cord sample was taken at the compression level C5. Histopathological assessment and immunohistochemistry of neurofilaments (NF), S-100, brain derived neurotrophic factor (BDNF), and evaluation of functional motoric outcome were done before animals were terminated. RESULTS: Chronic cervical myelopathy in rabbit model causes decreased expression of NF, S-100, BDNF, and decreased motor function. Oral administration of OLE increased the expression of these biomarkers and improved motor function outcomes. DISCUSSION: These findings indicate that OLE may be effective in protecting chronic cervical myelopathy in rabbit model.