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Cannabis (also known as marijuana) is the most frequently used psychoactive substance globally. Cannabis exerts therapeutic functions for many indications and has vast potential as a health and wellness product. Advances in our understanding of the composition and pharmacological properties of cannabis have revealed interactions between cannabis, an individuals’ circadian rhythms and their endocannabinoid signaling. Exogenously administered cannabinoids can bidirectionally entrain central and peripheral clocks that comprise circadian rhythms, and malfunctions in the endocannabinoid system are reported to impact neurological processes. Therefore, it is necessary to account for the circadian rhythm when designing clinical trials examining the pharmacological properties of cannabis-based products for health and wellness to limit its potential confounding impact on results. Consideration of the entrainment capabilities of the endocannabinoid system is warranted when designing clinical trials.

Introduction Guillain-Barré syndrome (GBS) is a worldwide demyelinating polyradiculopathy and polyneuropathy. Currently, there is no specific drug for GBS, and established treatment is generally based on immune-modulating treatment with plasma exchange or intravenous immunoglobulin in combination with supportive care. This study aimed to investigate the efficiency of integrated Chinese and Western medicine for acute GBS treatment. Methods We enrolled 73 subjects, and randomly divided them into two groups: 35 cases in the traditional Chinese medicine (TCM) group, and 28 in the Control group. The Control group was treated with the common Western medicine for one month; and the TCM group was administrated with one month of common treatment combined with TCM medication. Results Compared to the controls, TCM significantly enhanced the treatment efficiency in symptom expression, including the TCM syndrome score, the activity of daily living score, Hughes functional score and sensory dysfunction assessment. The total effective rate of the TCM group was 94.29%, significantly better than controls (78.59%). Moreover, TCM provide better improvement in motor nerve conduction functions (distal motor latency and motor conduction velocity) and sensory nerve conduction functions (sensory conduction velocity and sensory nerve action potential) in median nerve, ulnar nerve, and common fibular nerve. Conclusion When combined with TCM administration, the GBS treatment could acquire better outcomes.

Aim The aim of this study was to investigate the neuroprotective effects of hydrochloride fasudil (HF) in rats following intracerebral hemorrhage (ICH). Methods Male Wistar rats were randomly divided into four groups: normal, sham-operated, ICH, and ICH/HF. ICH was induced by injection of non-anticoagulant autologous arterial blood into the right caudate nucleus. The levels of Rho-associated protein kinase 2 (ROCK2) mRNA and protein around the site of the hematoma were measured by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay (ELISA), respectively. The levels of interleukin-6 and tumor necrosis factor-α in serum were detected by ELISA. The inflammatory cells and changes in the neuronal morphology around the hematoma were visualized using hematoxylin and eosin and Nissl staining. Brain edema was measured by comparing wet and dry brain weights. Results Following ICH, the levels of ROCK2 were significantly increased from day 1 to day 7. The levels of ROCK2 were significantly lower in rats treated with HF than in controls. The levels of inflammatory cytokines and brain water content were significantly higher in rats treated with HF than in controls. Administration of HF significantly reduced the levels of inflammatory cytokines and brain water content from day 1 to day 7. In the acute phase of ICH, a large number of neutrophils infiltrated the perihematomal areas. In comparison with the ICH group, the ICH/HF group showed markedly fewer infiltrating neutrophils on day 1. Nissl staining showed that ICH caused neuronal death and loss of neurons in the perihematomal areas at all time points and that treatment with HF significantly attenuated neuronal loss. Conclusions HF exerts neuroprotective effects in ICH rats by inhibiting the expression of ROCK2, reducing neutrophil infiltration and production of inflammatory cytokines, decreasing brain edema, and attenuating loss of neurons.

In fluorosis-endemic areas, exposure to high levels of fluoride causesneurotoxicity such as lowered intelligence and cognitive impairment. Oxidativedamage is critical to pathophysiologic processes of fluoride intoxication, andneurotoxicity of fluoride may be associated with oxidative stress. In previousstudies, maize purple plant pigment (MPPP), which was rich in anthocyanins,showed a strong scavenging activity in vitro and invivo . The present study aimed to determine whether treatment withMPPP can alleviate fluoride-induced oxidative damage in rat brain. After 3months of experiment, brain tissues were assayed for oxidative stress variables,histological and Western blotting examinations. Our results showed that MPPPreduced the elevated malondialdehyde levels, increased superoxide dismutaseactivity, and further attenuated histopathological alterations and mitigatedneuronal apoptosis. Importantly, MPPP also reversed changes in Bax and Bcl-2.Therefore, it was speculated that MPPP protects brain tissue from fluoridetoxicity through its antioxidant capacity.

Local field potentials (LFPs) are involved in almost all cognitive activities of animals. Several kinds of recording electrodes are used for recording LFPs in freely moving animals, including commercial and homemade electrodes. However, commercial recording electrodes are expensive, and their relatively fixed size often causes a steric hindrance effect, especially when combining deep brain stimulation (DBS) with LFP recording, which may not always satisfy the aim of researchers. Currently, an increasing number of researchers are designing their own recording electrodes to lower research costs. Nevertheless, there is no simple universal method to produce low-cost recording electrodes with a specific size according to the target brain area. Thus, we developed a simple method for quickly producing low-cost multiple-channel recording electrodes. To inspect the effectiveness of our self-designed electrode, LFPs were recorded in a Parkinson’s disease (PD) rat model, and an electrical stimulation electrode was implanted into the subthalamic nucleus to verify the space-saving ability of the self-designed recording electrode. The results showed that <30 min was needed to prepare an electrode and that the electrode materials cost <5 dollars. Further investigations showed that our electrode successfully recorded the beta oscillations (12–40 Hz) in the PD rat model. Thus, this method will greatly reduce the cost of recording electrodes and save time for researchers. Additionally, the small size of the electrode will further facilitate DBS research. Graphical Abstract

Objective This study was designed to investigate the indirect neuroprotective properties of recombinant human erythropoietin (rhEPO) pretreatment in a rat model of transient middle cerebral artery occlusion (MCAO). Methods One hundred and ten male Wistar rats were randomly assigned to four groups receiving either 5,000 IU/kg rhEPO intravenously or saline 15 minutes prior to MCAO and bilateral craniectomy or sham craniectomy. Bilateral craniectomy aimed at elimination of the space-consuming effect of postischemic edema. Diagnostic workup included neurological examination, assessment of infarct size and cerebral edema by magnetic resonance imaging, wet–dry technique, and quantification of hemispheric and local cerebral blood flow (CBF) by flat-panel volumetric computed tomography. Results In the absence of craniectomy, EPO pretreatment led to a significant reduction in infarct volume (34.83 ± 9.84% vs. 25.28 ± 7.03%; p = 0.022) and midline shift (0.114 ± 0.023 cm vs. 0.083 ± 0.027 cm; p = 0.013). We observed a significant increase in regional CBF in cortical areas of the ischemic infarct (72.29 ± 24.00% vs. 105.53 ± 33.10%; p = 0.043) but not the whole hemispheres. Infarct size-independent parameters could not demonstrate a statistically significant reduction in cerebral edema with EPO treatment. Conclusions Single-dose pretreatment with rhEPO 5,000 IU/kg significantly reduces ischemic lesion volume and increases local CBF in penumbral areas of ischemia 24 h after transient MCAO in rats. Data suggest indirect neuroprotection from edema and the resultant pressure-reducing and blood flow-increasing effects mediated by EPO.

Background The relationship between the apolipoprotein E ( APOE )- ε4 allele, triglyceride (TG) level, and cholesterol level and an increased risk of developing Alzheimer’s disease (AD) has been well established, but their relationship with behavioral-variant frontotemporal dementia (bvFTD) is not well-known. Methodology The levels of TGs, total cholesterol (TC), low-density lipoprotein (LDL), and high-density lipoprotein were measured in bvFTD and AD patients and in normal controls (NCs). DNA was extracted, and APOE was genotyped. Results The APOE-ε4 allele frequency was higher in the AD group than in the NC group, but no difference was found between the AD and the bvFTD groups. The bvFTD group had higher LDL than the AD group, and significant differences were also found for the cholesterol level in the dementia groups compared with the NC group. Elevated LDL level was positively correlated with appetite and eating score in the bvFTD group. Compared with the AD patients and NCs without the APOE-ε4 allele, those with the APOE-ε4 allele had higher TC, but its correlation with the bvFTD group was absent. Conclusions The bvFTD and the AD groups had higher cholesterol levels. The APOE-ε4 allele and eating behavior might modify lipid metabolism in dementia. TG and cholesterol analyses may offer a new opportunity for targeted treatments.

Objective The aim of this study is to investigate the dysbiosis characteristics of gut microbiota in patients with cerebral infarction (CI) and its clinical implications. Methods Stool samples were collected from 79 CI patients and 98 healthy controls and subjected to 16S rRNA sequencing to identify stool microbes. Altered compositions and functions of gut microbiota in CI and its correlation with clinical features were investigated. Random forest and receiver operating characteristic analysis were used to develop a diagnostic model. Results Microbiota diversity and structure between CI patients and healthy controls were overall similar. However, butyrate-producing bacteria (BPB) were significantly reduced in CI patients, while lactic acid bacteria (LAB) were increased. Genetically, BPB-related functional genes were reduced in CI patients, whereas LAB-related genes were enhanced. The interbacterial correlations among BPB in CI patients were less prominent than those in healthy controls. Clinically, BPB was negatively associated with the National Institutes of Health Stroke Scale (NIHSS), while LAB was positively correlated with NIHSS. Both BPB and LAB played leading roles in the diagnostic model based on 47 bacteria. Conclusions The abundance and functions of BPB in CI patients were significantly decreased, while LAB were increased. Both BPB and LAB displayed promising potential in the assessment and diagnosis of CI.

Introduction Spinal cord injury (SCI) leads to abnormal expression of miRs, leading to secondary responses such as oxidative stress, inflammation and apoptosis. In the present work, we screened the miRs involved and the associated pathway. Methods In a rat model of SCI, the microarray analysis for expression of miRs at various time points post-SCI was done. The locomotor analysis was done by Basso, Beattie and Bresnahan score, and Cresyl violet staining was done for lesion volume and TUNEL assay was done for apoptosis in neuronal cells. The expression of apoptotic proteins was done by the western blot study. Results It was evidenced that the expression of the number of miRs was altered on the 14th day post-SCI, and miR-142-3p was found to be the most significantly suppressed miR. The results suggested that overexpression of miR-142-3p by its agomir-attenuated functional recovery decreased lesion size and apoptosis of neuronal cells in rats subjected to SCI. The luciferase assay indicated that miR-142-3p blocked the levels of Bax, which is a significant activator of the mitochondrial apoptotic pathway (MAP) via targeting the 3′UTR region of BV-2 cells, and in addition, pc-DNA-Bax restored Bax and inhibited the correcting role of miR-142-3p in hydrogen peroxide-treated BV-2 cells. The findings suggested that miR-142-3p may inhibit the MAP by inhibiting the expression of cleaved-caspase-3/-9 and Bax in SCI rats. Conclusion This study concludes that miR-142-3p may attenuate the functional recovery and decrease apoptosis in neuronal cells via inhibiting the MAP in the spinal cord-injured rats, confirming miR-142-3p as a potential therapeutic target in treating SCI.

Background Fibrosis in the ventricular system is closely associated with post-hemorrhagic hydrocephalus (PHH). It is characterized by an expansion of the cerebral ventricles due to CSF accumulation following intraventricular hemorrhage (IVH). The activation of transforming growth factor-β1 (TGF-β1) may be involved in thrombin-induced arachnoid fibrosis. Methods A rat model of PHH was established by injection of autologous non-anticoagulated blood from the right femoral artery into the lateral ventricles. Differential expression of miR-30a was detected in rat arachnoid cells by RNA sequencing. AP-1, c-Fos, and TRAF3IP2 were knocked down in primary arachnoid cells, and the degree of arachnoid fibrosis was assessed. Results Decreased expression of miR-30a and increased expression of TRAF3IP2, TGF-β1, and α-SMA were detected in the arachnoid cells of PHH rat. Besides, overexpression of miR-30a targets TRAF3IP2 mRNA 3′UTR and inhibits the expression of TRAF3IP2, TGF-β1, and α-SMA in the primary arachnoid cells. Furthermore, TRAF3IP2 activates AP-1 to promote arachnoid fibrosis. The content of type I collagen in the primary arachnoid cells was reduced after the silencing of AP-1 and TRAF3IP2. Conclusions This study identified a miR-30a-regulated mechanism of arachnoid fibrosis, suggesting a previously unrecognized contribution of miR-30a to the pathogenesis of fibrosis in the ventricular system. These results might provide a new target for the clinical diagnosis and treatment of PHH.

Background: Amyloid-beta (Aβ) plaque deposits and neurofibrillary tangles containing tau proteins are the key pathognomonic manifestations of Alzheimer’s disease (AD). Lack of holistic drugs for AD has reinvigorated enthusiasm in the natural product-based therapies. In this study, our idea to decipher the beneficial effects of C-phycocyanin (CPC) in the management of AD is buoyed by its multifaceted and holistic therapeutic effects. Methods: We evaluated the effect of CPC treatment on epigenetic factors and inflammatory mediators in a mouse with oligomeric Aβ 1-42 -induced AD. Besides, the cognitive function was evaluated by the spatial memory performance on a radial arm maze. Results: The results showed cognitive deficit in the mice with AD along with upregulated HDAC3 expression and diminished miRNA-335 and brain-derived neurotrophic factor (BDNF) expressions. In addition, inflammation was provoked (manifested by increased interleukins (IL)-6 and IL-1β) and neuronal apoptosis was accelerated (indicated by increased Bax, caspase-3, and caspase-9 along with decreased Bcl2) in the hippocampus of the mice with AD. Interestingly, CPC treatment in the mice with AD improved spatial memory performance and decreased the perturbations in the epigenetic and inflammatory biofactors. Conclusion: These results underscore that mitigation of inflammation via regulation of epigenetic factors might be the key pathway underlying the ameliorative effect of CPC against the aberrations in AD. Our findings provide the rationale for considering CPC as a viable therapeutic option in the management of AD.

Background Spinal cord injury (SCI) causes devastating loss of function and neuronal death without effective treatment. (−)-Epigallocatechin-3-gallate (EGCG) has antioxidant properties and plays an essential role in the nervous system. However, the underlying mechanism by which EGCG promotes neuronal survival and functional recovery in complete spinal cord transection (ST) remains unclear. Methods In the present study, we established primary cerebellar granule neurons (CGNs) and a T10 ST rat model to investigate the antioxidant effects of EGCG via its modulation of protein kinase D1 (PKD1) phosphorylation and inhibition of ferroptosis. Results We revealed that EGCG significantly increased the cell survival rate of CGNs and PKD1 phosphorylation levels in comparison to the vehicle control, with a maximal effect observed at 50 µM. EGCG upregulated PKD1 phosphorylation levels and inhibited ferroptosis to reduce the cell death of CGNs under oxidative stress and to promote functional recovery and ERK phosphorylation in rats following complete ST. Conclusion Together, these results lay the foundation for EGCG as a novel strategy for the treatment of SCI related to PKD1 phosphorylation and ferroptosis.

Oxidative stress, abnormal fatty acid metabolism, and impaired gut microbiota play a serious role in the pathology of autism. The use of dietary supplements to improve the core symptoms of autism is a common therapeutic strategy. The present study analyzed the effects of oral supplementation with Novavit, a multi-ingredient supplement, on ameliorating oxidative stress and impaired lipid metabolism in a propionic acid (PPA)-induced rodent model of autism. Male western albino rats were divided into three groups. The first group is the control, the second group was given an oral neurotoxic dose of PPA (250 mg/kg body weight/day) for 3 days and then received buffered saline until the end of the experiment. The third group received Novavit (70 mg/kg body weight/day for 30 days after the 3-day PPA treatment). Markers of oxidative stress and impaired fatty acid metabolism were measured in brain homogenates obtained from each group. Novavit modulation of the gut microbiota was also evaluated. While PPA induced significant increases in lipid peroxides and 5-lipoxygenase, together with significantly decreased glutathione, and cyclooxygenase 2, oral supplementation with Novavit ameliorated PPA-induced oxidative stress and impaired fatty acid metabolism. Our results showed that the presence of multivitamins, coenzyme Q10, minerals, and colostrum, the major components of Novavit, protects against PPA-induced neurotoxicity.

Obesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione- s -transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group ( P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

The purpose of this study was to quantify head motion between isometric erector spinae (ES) contraction strategies, paradigms, and intensities in the development of a neuroimaging protocol for the study of neural activity associated with trunk motor control in individuals with low back pain. Ten healthy participants completed two contraction strategies; (1) a supine upper spine (US) press and (2) a supine lower extremity (LE) press. Each contraction strategy was performed at electromyographic (EMG) contraction intensities of 30, 40, 50, and 60% of an individually determined maximum voluntary contraction (MVC) (±10% range for each respective intensity) with real-time, EMG biofeedback. A cyclic contraction paradigm was performed at 30% of MVC with US and LE contraction strategies. Inertial measurement units (IMUs) quantified head motion to determine the viability of each paradigm for neuroimaging. US vs LE hold contractions induced no differences in head motion. Hold contractions elicited significantly less head motion relative to cyclic contractions. Contraction intensity increased head motion in a linear fashion with 30% MVC having the least head motion and 60% the highest. The LE hold contraction strategy, below 50% MVC, was found to be the most viable trunk motor control neuroimaging paradigm.

Background Sevoflurane, a volatile anesthetic, is known to induce widespread neuronal degeneration and apoptosis. Recently, the stress-inducible protein sestrin 2 and adenosine monophosphate-activated protein kinase (AMPK) have been found to regulate the levels of intracellular reactive oxygen species (ROS) and suppress oxidative stress. Notoginsenoside R1 (NGR1), a saponin isolated from Panax notoginseng , has been shown to exert neuroprotective effects. The effects of NGR1 against neurotoxicity induced by sevoflurane were assessed. Methods Sprague-Dawley rat pups on postnatal day 7 (PD7) were exposed to sevoflurane (3%) anesthesia for 6 h. NGR1 at doses of 12.5, 25, or 50 mg/kg body weight was orally administered to pups from PD2 to PD7. Results Pretreatment with NGR1 attenuated sevoflurane-induced generation of ROS and reduced apoptotic cell counts. Western blotting revealed decreased cleaved caspase 3 and Bad and Bax pro-apoptotic protein expression. NGR1 substantially upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) expression along with increased heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase-1 levels, suggesting Nrf2 signaling activation. Enhanced sestrin-2 and phosphorylated AMPK expression were noticed following NGR1 pretreatment. Conclusion This study revealed the neuroprotective effects of NGR1 through effective suppression of apoptosis and ROS via regulation of apoptotic proteins and activation of Nrf2/HO-1 and sestrin 2/AMPK signaling cascades.

Background Inflammation is involved in cerebral ischemia/reperfusion (I/R)-induced neurological damage. Saikosaponin A (SSa), extracted from Radix bupleuri , has been reported to exert anti-inflammatory effects. This article aimed to investigate whether SSa could ameliorate neuroinflammation mediated by ischemic stroke and the underlying mechanism. Methods Rat middle cerebral artery occlusion (MCAO) model was employed in this study, and the cognitive and motor functions were detected by behavioral tests. Inflammatory cytokines in the serum were detected by ELISA kits. The expression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and high-mobility group box 1 (HMGB1) in the brain tissues were assayed with Western blot. Results Our results showed that SSa pretreatment could significantly reduce brain damage, improve neurological function recovery, and decrease the water content of brain tissues when compared with the model group. SSa pretreatment significantly reduced the serum HMGB1 level and downregulated the contents of inflammatory cytokines including tumor necrosis factor-α, interleukin-1 beta, and interleukin-6. Furthermore, SSa pretreatment could attenuate the decreased TLR4 and nucleus NF-κB in the brain of MCAO rats. The protein level of HMGB1 in the nucleus was significantly upregulated in the SSa pretreatment group. Conclusion Our results suggested that the pretreatment with SSa provided significant protection against cerebral I/R injury in rats via its anti-inflammation property by inhibiting the nucleus HMGB1 release.

Transcription factor EB (TFEB)-based gene therapy is a promising therapeutic strategy in treating neurodegenerative diseases by promoting autophagy/lysosome-mediated degradation and clearance of misfolded proteins that contribute to the pathogenesis of these diseases. However, recent findings have shown that TFEB has proinflammatory properties, raising the safety concerns about its clinical application. To investigate whether TFEB induces significant inflammatory responses in the brain, male C57BL/6 mice were injected with phosphate-buffered saline (PBS), adeno-associated virus serotype 8 (AAV8) vectors overexpressing mouse TFEB (pAAV8-CMV-mTFEB), or AAV8 vectors expressing green fluorescent proteins (GFPs) in the barrel cortex. The brain tissue samples were collected at 2 months after injection. Western blotting and immunofluorescence staining showed that mTFEB protein levels were significantly increased in the brain tissue samples of mice injected with mTFEB-overexpressing vectors compared with those injected with PBS or GFP-overexpressing vectors. pAAV8-CMV-mTFEB injection resulted in significant elevations in the mRNA and protein levels of lysosomal biogenesis indicators in the brain tissue samples. No significant changes were observed in the expressions of GFAP, Iba1, and proinflammation mediators in the pAAV8-CMV-mTFEB-injected brain compared with those in the control groups. Collectively, our results suggest that AAV8 successfully mediates mTFEB overexpression in the mouse brain without inducing apparent local inflammation, supporting the safety of TFEB-based gene therapy in treating neurodegenerative diseases.

Peripheral nerve injury is a life-changing disability with significant socioeconomic consequences. In this rat model, we propose that partial enzyme digestion can facilitate the functional recovery of a crushed nerve. The sciatic nerves were harvested and in vitro cultured with the addition of Liberase to determine the appropriate enzyme amount in the hyaluronic acid (HA) membrane. Then, the sciatic nerve of adult male Sprague-Dawley rats was exposed, crushed, and then treated with partial enzyme digestion (either 0.001 or 0.002 unit/mm 2 Liberase-HA membrane). The sciatic function index (SFI) for functional recovery of the sciatic nerve was evaluated. After 2 h of in vitro digestion, fascicles and axons were separated from each other, with the cells mobilized. Greater destruction of histology structures occurred in the high enzyme (Liberase-HA membrane at 0.002 unit/mm 2 ) group at 24 h than in the low enzyme (0.001 unit/mm 2 ) group at 48 h. In the SFI evaluation, the improvement in 0.001 unit/mm 2 Liberase group was significantly better than control and 0.002 unit/mm 2 Liberase group. Our study demonstrated that appropriate enzyme digestion had a significantly faster and earlier recovery.

Background We tested the hypothesis whether there is a correlation between the echogenicity and calcium and water contents of carotid plaques. Patients and methods Ninety carotid befurcations from 45 deceased patients were removed during autopsy. Thirty-four plaques were categorized as homogenous echolucent (HEL), homogenous echogenic (HEG) and heterogenous (HE) plaques based on premortem B-mode image. Water content was expressed in % of wet weight. Ca was determined by proton-induced X-ray emission and expressed in ppm. Relative optical density of the B-mode images was analyzed offline using a computer program. Results HEL plaques had lower Ca content (medians and IQRs: 6,145 [4,465–6,536 ppm]) compared to HEG (74,100 [15,300–1,44,500−ppm]), P ≤ 0.001). HE plaques showed an intermediate calcium content (7,310 [4,840–9,920 ppm]) that was statistically not different from echolucent plaques. Water content of HEG plaques was statistically not different from HEL and HE (HEG:53.5 [35.5–64%], HEL: 73.5 [69.7–78.5%], HE: 70.6 [67.4–73.9%]). HEG plaques had the highest relative optical densities (196 [188–217%]). HEL and HE had similar relative optical densities (HEL: 176 [164–187%], HE: 164 [144–188%], respectively). A significant positive correlation was found between the Ca content and relative optical density of plaques. Conclusions Echogenicity of carotid plaques increases along with their calcium content. Water content may be an important factor in differentiation of different plaques.

Background This retrospective study evaluated whether diabetes affects motor outcome after stroke by analyzing the effects of diabetes on motor prognosis by controlling for critical factors, including lesion type and location, corticospinal tract (CST) state, patient age, lesion volume, and treatment method during the stroke. Methodology We recruited 221 patients with intracerebral hemorrhage (ICH) of the basal ganglia. We used diffusion tensor tractography to investigate the CST state. We also evaluated the hemorrhage volume. We obtained information on the presence of diabetes and age by chart review. Motor outcomes at 6 months were measured using the upper and lower limb motricity index (MI), modified Brunnstrom classification (MBC), and functional ambulation category (FAC). We used multiple linear regression tests to investigate whether diabetes affected motor outcomes after stroke after adjusting for other factors, including CST state, age, lesion volume, and treatment method. Results The presence of diabetes was not correlated with motor outcome measurements, including upper and lower MIs, MBC, and FAC, at 6 months after the onset. However, the CST state, age, lesion volume, and treatment method were significantly correlated with nearly all motor outcomes. Conclusions We found that diabetes did not significantly affect motor outcomes after ICH.

Background Interferon regulatory factor 8 (IRF8) is involved in the pathogenesis of neuropathic pain. However, whether and how IRF8 can regulate the nicotine withdrawal (NTW)-induced hyperalgesia has not been clarified. Methods C57BL/6 mice were randomized and injected subcutaneously with saline (Control) or nicotine (3 mg/kg) three times per day for 7 consecutive days, followed by injection with mecamylamine to induce NTW. Their paw withdrawal latencies (PWLs) were measured, and the relative levels of IRF8 expression in the spinal cord tissues were determined longitudinally by western blot. The numbers of IRF8+ cells in the spinal cord tissues were examined. In addition, the NTW mice were randomized and infused intrathecally with vehicle saline (NS), control lentivirus or lentivirus for the expression of IRF8-specific shRNA for three days. Their PWLs, microglia activation, IRF8 and P2X4R and BDNF expression in the spinal cord tissues were determined. Results In comparison with the Control mice, the NTW significantly decreased the PWLs but increased the relative levels of IRF8 expression and the numbers of IRF8+ cells in the spinal cord tissues of mice. IRF8-silencing significantly mitigated the NTW-decreased PWLs and attenuated the NTW-enhanced microglia activation and P2X4R and BDNF expression in the spinal cord tissues of mice. Conclusions Spinal IRF8 is crucial for the NTW-induced hyperalgesia by enhancing microglia activation and spinal P2X4R and BDNF expression in mice. The IRF8/P2X4R/BDNF axis may be potential therapeutic targets for postoperative pain of smokers.

Introduction Skeletal muscle loss induces a poor rehabilitation outcome after stroke. Little is known about the usefulness of diffusion tensor tractography (DTT) findings of the corticospinal tract (CST) in terms of predicting muscle loss in affected limbs after stroke. Methods This research was designed as a preliminary study. Forty-four patients, with stroke onset more than one year earlier, were recruited. DTT was performed within 7–30 days after stroke onset. The patients were classified into two groups based on the DTT findings: a DTT+ group, in which the CST was preserved, and a DTT− group, in which the CST was interrupted by the stroke lesion. Additionally, the patients’ functions were evaluated based on the modified Brunnstrom classification and functional ambulation category. Results In the DTT− group, the values of the lean tissue mass of the affected upper and lower limbs were smaller than those of the unaffected side. On the other hand, in the DTT+ group, the values of the lean tissue mass between the affected and unaffected limbs were not significantly different. Conclusion The DTT evaluation of CST at the early stage of stroke may be useful for predicting muscle loss of the affected limb at the chronic stage in stroke patients.

Interleukin-27 (IL-27), which belongs to IL-12 family, influences the function of T cells (Tregs) through regulating the expression, and function of forkhead box P3 (FoxP3). In this study, we detected the IL-27 serum levels in 59 myasthenia gravis (MG) patients and 35 healthy controls (HCs). Among them, 32 MG patients received immunoglobulin intravenous (IVIG) injections (0.4 g/kg per day for 5 consecutive days). IL-27 levels were collected before and after the treatments and subjected to a comparative study. Finally, we assessed the correlations of IL-27 levels with the clinical characteristics of MG. As a result, serum IL-27 levels were significantly higher in MG patients than those in the HCs. Meanwhile, significant reduction was detected after the IVIG treatment. IL-27 levels positively correlated with both MG activities of daily living and quantitative MG score. IL-27 may participate in the pathogenesis of MG and can be used as an early marker for the diagnosis and prognosis of MG. In addition, IL-27 can be used as a target for MG treatment through the regulation of specific immune signaling and maintaining immune homeostasis.

Background Blood–brain barrier (BBB) dysfunction and neuroinflammation induced by traumatic brain injuries (TBIs) cause a succession of secondary brain damage events and finally lead to a massive and progressive cerebral neuronal destruction. Artesunate, a semisynthetic artemisinin derivative, is a potential candidate for the management of cerebral damage induced by TBI due to its protective function to BBB and cerebral neurons. Methods To demonstrate the effect of artesunate to TBI-induced BBB dysfunction and neural damage, TBI rat model was constructed by cortical impact injury. Behavioral experiments were used to estimate the impact of the combined treatment on rats. Western blotting was performed to demonstrate the protein levels in the brain tissues of rats. Quantitative real-time PCRs were utilized to investigate the alteration in the expression of various RNA levels. The chemokine levels were estimated by ELISA. Results Artesunate treatment attenuated the impact caused by TBI on rat brain and improved the long-term neurological recover. Artesunate treatment protected the integrity of BBB and inhibited neuroinflammation. Artesunate treatment promoted the phosphorylation of Akt and inhibited the phosphorylation of glycogen synthase kinase (GSK)-3β in TBI rat model. Conclusion Artesunate protected rats from TBI-induced impairments of BBB and improved longer-term neurological outcomes.

Background Alzheimer’s disease (AD) is a common neurodegenerative disorder without any satisfactory therapeutic approaches. AD is mainly characterized by the deposition of β-amyloid protein (Aβ) and extensive neuronal cell death. Curcumin, with anti-oxidative stress (OS) and cell apoptosis properties, plays essential roles in AD. However, whether bisdemethoxycurcumin (BDMC), a derivative of curcumin, can exert a neuroprotective effect in AD remains to be elucidated. Methods In this study, SK-N-SH cells were used to establish an in vitro model to investigate the effects of BDMC on the Aβ 1–42 -induced neurotoxicity. SK-N-SH cells were pretreated with BDMC and with or without compound C and EX527 for 30 min after co-incubation with rotenone for 24 h. Subsequently, western blotting, cell viability assay and SOD and GSH activity measurement were performed. Results BDMC increased the cell survival, anti-OS ability, AMPK phosphorylation levels and SIRT1 in SK-N-SH cells treated with Aβ 1–42 . However, after treatment with compound C, an AMPK inhibitor, and EX527, an SIRT1inhibitor, the neuroprotective roles of BDMC on SK-N-SH cells treated with Aβ 1–42 were inhibited. Conclusion These results suggest that BDMC exerts a neuroprotective role on SK-N-SH cells in vitro via AMPK/SIRT1 signaling, laying the foundation for the application of BDMC in the treatment of neurodegenerative diseases related to AMPK/SIRT1 signaling.

Objectives We investigated injuries of the optic radiations (ORs) in patients with mild traumatic brain injury (TBI) by using diffusion tensor tractography (DTT). Methods Fifty-two consecutive patients who complained of visual problems showed abnormal visual evoked potential (VEP) latency but no abnormality on conventional brain MRI after mild TBI, and fifty normal control subjects were recruited for this study. Subjects’ ORs were reconstructed using DTT, and three DTT parameters (fractional anisotropy [FA], apparent diffusion coefficient [ADC], and tract volume) were measured for each OR. Results Mean FA value and tract volume of the OR were significantly lower in the patient group than in the control group ( p < 0.05). However, there was no significant difference in the ADC values of the OR between the patient and control groups ( p > 0.05). A weak negative correlation was detected between VEP latency and OR fiber number ( r = 0.204, p < 0.05). Conclusions DTT revealed that OR injuries were not detected on the conventional brain MRI scans of patients who complained of visual problems and had abnormal VEP latency after mild TBI. Our results suggest that DTT would be a useful technique for detecting OR injury in patients with mild TBI.

Food consumption during the rest phase promotes circadian desynchrony, which is corrected with harmful physiological and mental disorders. Previously, we found that circadian desynchrony was involved in isoflurane-induced cognitive impairment. Here, we scheduled food access to modulate daily rhythm to examine its impact on isoflurane-induced cognitive impairments. Mice were randomly transferred to restricted feeding (RF) time groups: Control group (Zeitgeber time (ZT) 0–ZT24, ad libitum feeding), Day-Feeding group (ZT0–ZT12, misaligned feeding), and Night-Feeding group (ZT12–ZT24, aligned feeding). Then, some of them were subjected to 5 h of 1.3% isoflurane anaesthesia from ZT14 to ZT19 and were divided into the Control + Anes group, the Day-Feeding + Anes group, and the Night-Feeding + Anes group. Mini-Mitter was used to monitor the daily rhythm. Fear conditioning system was conducted to assess cognition of mice. We observed that the Night-Feeding group adapted to RF gradually, whereas the Day-Feeding group exhibited a disturbed daily rhythm. The Night-Feeding + Anes group exhibited a partially enhanced daily rhythm, whereas the Day-Feeding + Anes group exhibited sustained phase advances and diurnality score increase 7 days after isoflurane anaesthesia. Notably, in tests of hippocampus-dependent contextual memory, the Night-Feeding + Anes group demonstrated decreased deficits; the Day-Feeding + Anes group showed prolonged post-anaesthetic deficits 14 days after isoflurane anaesthesia. However, amygdala-dependent cued-fear conditioning post-anaesthesia was not altered by the RF schedule. In conclusion, we demonstrated that misaligned feeding disturbed the daily rhythm and led to persistent post-anaesthetic cognitive dysfunction. Aligned feeding enhanced the daily rhythm partially and improved post-anaesthetic cognitive dysfunction.

Objective Digital subtraction angiography (DSA) is considered the gold standard for cerebral vasculature observation and is increasingly applied among the elderly population. The aim of this study is to determine whether the use of a video-based education system can improve the image quality of percutaneous cerebral angiography. Method This study is a single-blinded prospective cohort trial. One hundred and sixty patients (≥65 years old) were enrolled in this study. Eighty patients were provided with video-based education as intervention. Eighty age-matched controls only received regular education. The DSA image quality was assessed between control and intervention groups. It was rated by two readers on a 5-point scale, independently. Results No differences were found between control and intervention groups in baseline characteristics ( P > 0.05). The mean overall image quality was significantly higher in patients receiving video-based education than in controls ( P < 0.05), and the same trends were found in the respective assessment of each artery (left and right carotid/vertebral artery; P < 0.05). Moreover, the operation time and radiation doses were quite comparable between the two groups ( P > 0.05). Conclusions This study indicated that video-based education helps elderly patients to acquire improved DSA image quality. It encourages the application of this approach in practice.

Background Therapeutic management of pain in patients with complex regional pain syndrome (CRPS) is challenging. Repetitive transcranial magnetic stimulation (rTMS) has analgesic effects on several types of pain. However, its effect on CRPS has not been elucidated clearly. Therefore, we conducted a meta-analysis of the available clinical studies on rTMS treatment in patients with CRPS. Materials and methods A comprehensive literature search was conducted using the PubMed, EMBASE, Cochrane Library, and SCOPUS databases. We included studies published up to February 09, 2020, that fulfilled our inclusion and exclusion criteria. Data regarding measurement of pain using the visual analog scale before and after rTMS treatment were collected to perform the meta-analysis. The meta-analysis was performed using Comprehensive Meta-analysis Version 2. Results A total of three studies (one randomized controlled trial and two prospective observational studies) involving 41 patients were included in this meta-analysis. No significant reduction in pain was observed immediately after one rTMS treatment session or immediately after the entire schedule of rTMS treatment sessions (5 or 10 sessions; P > 0.05). However, pain significantly reduced 1 week after the entire schedule of rTMS sessions ( P < 0.001). Conclusion rTMS appears to have a functional analgesic effect in patients with CRPS.

Intracranial hemorrhage (ICH) causes high mortality and disability without effective treatment in the clinical setting. (−)-Epigallocatechin-3-gallate (EGCG) exerts an essential role in the central nervous system and offers a promising therapeutic agent for the treatment of oxidative damage-related diseases. MiR-137 can inhibit the oxidative stress and apoptosis to attenuate neuronal injury. However, the role of EGCG in regulating miR-137-3p and neuronal Parthanatos remains to be unclear. In the present study, we build the ICH mice model to investigate the antioxidant effects of EGCG via upregulating miR-137-3p and inhibiting neuronal Parthanatos. We revealed that EGCG upregulated miR-137-3p and inhibited neuronal Parthanatos, and promoted the functional recovery, alleviated ICH-induced brain injury, and reduced oxidative stress in mice following ICH. However, following the inhibition of miR-137-3p and activation of Parthanatos, EGCG was unable to exert neuroprotective roles. These combined results suggest that EGCG may upregulate miR-137-3p and inhibit neuronal Parthanatos to accelerate functional recovery in mice after ICH, laying the foundation for EGCG to be a novel strategy for the treatment of neuronal injuries related to Parthanatos.

Objective To investigate the effect and medical imaging of modified hemispherectomy on patients with infantile hemiparesis and medically refractory epilepsy. Patients and methods Forty-three patients with infantile hemiparesis and refractory epilepsy who underwent hemispherectomy were enrolled. The treatment effect and medical imaging were analyzed. Results Anatomical hemispherectomy was successfully performed in all patients (100%). In all patients, the muscular tension decreased and the contracted limbs relaxed. In the pathological examination of the resected brain tissue, secondary cicatricial gyri with concomitant cortical dysplasia was present in 36 cases and polycerebellar gyrus malformation and porencephalia in the other 7 cases. Followed up for 7–15 years (mean 11.3), all patients were alive without a long-term sequela. Epilepsy was satisfactorily controlled, with complete seizure relief in 39 cases (91%) classified as Engel I and basic control in the other 4 (9%) defined as Engel II. The posthemispherectomy medical imaging demonstrated that the intracranial space on the operative side shrank, and the healthy cerebral hemisphere shifted markedly toward the hemispherectomy side, with expanded lateral ventricle on the healthy side and thickened skull and enlarged frontal sinus on the operative side. After 4–5 years, the intracranial space on the operative side disappeared in 75% of the patients, demonstrating enlarged cerebral peduncle on the healthy side. Conclusion Further modified hemispherectomy in patients with infantile hemiparesis and medically refractory epilepsy demonstrated markedly ameliorated effects on epilepsy control and the prevention of superficial cerebral hemosiderosis in the long-term follow-up.

Background: Alzheimer’s disease (AD) is an ultimately fatal, degenerative brain disease in the elderly people. In the current work, we assessed the defensive capability of isovitexin (IVX) through an intracerebroventricular injection of streptozotocin (STZ)-induced AD mouse model. Methods: Mice were separated into four cohorts: sham-operated control mice; STZ-intoxicated Alzheimer’s mice; IVX cohort, IVX + STZ; and Ant-107 cohort, antagomiR-107 + IVX/STZ as in the IVX cohort. Results: The outcomes indicated that IVX administration ameliorated spatial memory loss and blunted a cascade of neuro-noxious episodes – including increased amyloid-beta (Aβ) and degraded myelin basic protein burden, neuroinflammation (represented by elevated caspase-1, TNF-α and IL-6 levels) and autophagic dysfunction (represented by altered LC3-II, Atg7 and beclin-1 expressions) – via the inhibition of PI3K/Akt/mTOR signalling axis. We considered the question of whether the epigenetic role of microRNA-107 (miR-107) has any impact on these events, by using antagomiR-107. Conclusion: This probing underscored that miR-107 could be a pivotal regulatory button in the activation of molecular signals linked with the beneficial autophagic process and anti-inflammatory activities in relation to IVX treatment. Hence, this report exemplifies that IVX could guard against Aβ toxicity and serve as an effectual treatment for patients afflicted with AD.

Deep brain stimulation (DBS) applied to the nucleus accumbens (NAc) alleviates the depressive symptoms of major depressive disorders. We investigated the mechanism of this effect by assessing gene expression and RNA methylation changes in the ventral tegmental area (VTA) following NAc-DBS in a chronic unpredictable mild stress (CUMS) mouse model of depression. Gene expression and N 6 -methyladenosine (m 6 A) levels in the VTA were measured in mice subjected to CUMS and then DBS, and transcriptome-wide m 6 A changes were profiled using immunoprecipitated methylated RNAs with microarrays, prior to gene ontology analysis. The expression levels of genes linked to neurotransmitter receptors, transporters, transcription factors, neuronal activities, synaptic functions, and mitogen-activated protein kinase and dopamine signaling were upregulated in the VTA upon NAc-DBS. Furthermore, m 6 A modifications included both hypermethylation and hypomethylation, and changes were positively correlated with the upregulation of some genes. Moreover, the effects of CUMS on gene expression and m 6 A-mRNA modification were reversed by DBS for some genes. Interestingly, while the expression of certain genes was not changed by DBS, long-term stimulation did alter their m 6 A modifications. NAc-DBS-induced modifications are correlated largely with upregulation but sometimes downregulation of genes in CUMS mice. Our findings improve the current understanding of the molecular mechanisms underlying DBS effects on depression.

Background Sudoku is a popular cognitively stimulating leisure-time activity. Many studies have been directed toward finding an algorithm to solve Sudoku, but the investigation of the neural substrates involved in Sudoku has been challenging. Methods Sudoku task was divided into two steps to understand the differential function of the prefrontal cortex (PFC) while applying heuristic rules. PFC activity was recorded at 16 optode locations using functional near infrared spectroscopy. Classical two-way analysis of variance as well as general linear model-based approach was used to analyze the data from 28 noise-free recordings obtained from right-handed participants. Results Post hoc analysis showed a significant increase in oxyhemoglobin concentrations and decrease in deoxyhemoglobin concentrations at all 16 optode locations during step 1 (3 × 3 subgrids) and step 2 (easy level 9 × 9 Sudoku) when compared with the rest ( p < 0.0001). Contrasting the step 2 – step 1 revealed that medial regions of PFC were preferentially activated. Conclusion Both the medial and lateral regions of PFC are activated during Sudoku task. However, the medial regions of PFC play a differential role, especially when we consider searching and selecting the heuristic rules. Thus, Sudoku may be used for cognitive remediation training in neuropsychiatric disorders involving PFC. Graphical abstract

Background The aim of this study was to investigate the neural plasticity in contralesional cortex and the effects of tongxinluo (TXL) in cerebral ischemic rats. Methodology We used stroke-prone renovascular hypertensive (RHRSP) cerebral ischemia rat models to study the effect of TXL and the underlying mechanisms. We performed foot-fault and beam-walking tests to evaluate the motor function of rats after cortical infarction. Biotinylated dextran amine (BDA) was used to track axonal sprouting and neural connections. Results TXL enhanced the recovery of motor function in cerebral infarction rats. TXL increased axonal sprouting in the peri-infarcted area but not in the corpus callosum, indicating in situ origination instead of crossing between cortical hemispheres through the corpus callosum. TXL promoted the sprouting of corticospinal axons into the denervated side of spinal gray matter. The synaptophysin (SYN)-positive intensity in the peri-infarcted area of TXL-treated group was greater than that in the vehicle group. We observed co-localization of SYN with BDA-positive fibers in the denervated spinal cord gray matter in the TXL group, suggesting that axonal remodeling and synaptic connections were promoted by TXL. Conclusion TXL may promote the recovery of neurological function by promoting the axonal remodeling and synapse formation of motor neuronal fibers after focal cortical infarction in hypertensive rats.

Background This study investigated the therapeutic potential of eriodictyol (EDC) in spinal cord injury (SCI) rats and also the mechanism involved. Methods The SCI model was created in Sprague-Dawley rats by the weight drop method. The SCI rats were divided into four groups, namely, Sham operated group (submitted for laminectomy only), control rats (vehicle treated), rats treated with 10 mg/kg EDC and rats treated with 20 mg/kg EDC. EDC or vehicle was injected in The SCI rats via subarachnoid route at the lumbar level 4 just after inducing SCI. The open field and inclined plane tests were done for assessing the locomotor activity. Histopathological analysis of the injured site of the spinal cord was done. Western blot analysis and immunohistochemical analysis were done for the expression of Bcl-2, Bax, glial cell line–derived neurotrophic factor (GCDNF) and brain-derived neurotrophic factor (BDNF). Results The outcomes suggested that EDC-treated rats showed significant improvement in the locomotor activity and also exhibited low myelin loss. The rats also showed overexpression of Bcl-2 and Bax. The treatment of EDC also increased the levels of GCDNF and BDNF after SCI. These outcomes suggested that EDC exerted the neuroprotective effect and also improved the locomotor activity by improving the levels of GCDNF and BDNF and blocking the apoptosis-related proteins. Conclusion This study suggests that EDC could ameliorate the locomotor function, and the neuroprotective action may be attributed to modulation of GCDNF and BDNF and blockade of apoptosis-associated proteins.

Objective The aim of this study was to explore, in a sample population of people with schizophrenia (PWS), the role of the anticholinergic burden on the perception of oral health-related quality of life (OHrQoL) in France. Methods A pilot study was performed between March 2014 and January 2016. PWS were recruited from a population in Côte d’Or department in France. Dental status was investigated using the Decayed, Missing, or Filled Teeth (DMFT) index, the Xerostomia Index (XI), and the Global Oral Health Assessment Index (GOHAI) for OHrQoL. The anticholinergic impregnation score was recorded using the anticholinergic impregnation scale (AIS). Results A sample of 62 people was selected. The DMFT score was 16.5± 8.7, the XI score was 22.9±7.8, the GOHAI score was 43.0±8.8, and the AIS score was 3.1±2.8. In total, 169 drugs were prescribed to the people of our sample, and 114 different anticholinergic drugs were observed. The most frequently used anticholinergic drugs (51.40%), in the study had a low antimuscarinic potency (1 point according to AIS scale). The multiple linear regression model showed that the OHrQoL scores were significantly lower when the DMFT scores, XI score, and anticholinergic scores were high. Conclusions This pilot study highlighted the potential role of the anticholinergic burden on the OHrQoL of PWS. A study with a validated specific scale for the OHrQoL and a standard anticholinergic burden scale should be conducted to clarify the role of anticholinergic drugs on the OHrQoL for PWS.

Objectives Aberrant cortical development, inferred from cortical folding, is linked to the risk of schizophrenia. Cortical folds develop in a time-locked fashion during fetal growth. We leveraged this temporal specificity of sulcation to investigate the timing of the prenatal insult linked to schizophrenia and the cognitive impairment seen in this illness. Methods Anatomical MRI scans from 68 patients with schizophrenia and 72 controls were used to evaluate the sulcal depth of five major invariable primary sulci representing lobar development (calcarine sulcus, superior temporal sulcus, superior frontal sulcus, intraparietal sulcus and inferior frontal sulcus) with formation representing the distinct developmental periods. Results A repeated-measure ANOVA with five sulci and two hemispheres as the within-subject factors and gender, age and intracranial volume as covariates revealed a significant effect of diagnosis ( F [1,134] = 14.8, p = 0.0002). Control subjects had deeper bilateral superior temporal, right inferior frontal and left calcarine sulci. A deeper superior frontal sulcus predicted better cognitive scores among patients. Conclusion Our results suggest that the gestational disruption underlying schizophrenia is likely to predate, if not coincide with the appearance of calcarine sulcus (early second trimester). Nevertheless, the burden of cognitive deficits may relate specifically to the aberrant superior frontal development apparent in late second trimester.

Primary central nervous system lymphoma (PCNSL) is rare. And the symptoms of PCNSL are atypical, it is extremely easy to be misdiagnosed as other diseases. However, early treatment is crucial which is requesting early diagnosis. We report a case of a 47-year-old man who was initially diagnosed as neuromyelitis optica (NMO) on the basis of clinical findings, slightly high Aquaporin4 (AQP4) (1:10) and high signals of magnetic resonance imaging. Though his symptoms progressively improved after steroid pulse treatment, but worse when steroid was decreased to 40 mg per day. We considered the patient should be diagnosed as PCNSL. After the examination of magnetic resonance spectroscopy (MRS) and positron emission tomography (PET), the results indicated PCNSL was most possible. Therefore we gave him stereotactic biopsy of deep of supratentorial, which showed non-Hodgkin malignant B-cell lymphoma.

Movement disorders post-amputation are a rare complication and can manifest as the jumping stump phenomenon, a form of peripheral myoclonus. The pathophysiology remains unknown and there is currently no standardized treatment. We describe the case of a 57-year-old male with unremitting stump myoclonus, starting one month after transtibial amputation, in his residual limb without associated phantom or neurological pain. The consequence of the myoclonus was a reduction in prosthetic wearing time. Failure to respond to oral medication led us to attempt the use of botulinum neurotoxin Type A injections in the involved muscles of the residual limb. Injection trials, over a two-year period, resulted in an improvement of movement disorder, an increased prosthetic wearing time and a higher satisfaction level of the patient. Injection of botulinum toxin type A should be considered as an alternative treatment for stump myoclonus to improve prosthetic wearing time and comfort.

Reversible splenial lesion syndrome (RESLES) is a single-stage non-specific syndrome with unclear pathogenesis. There has been no report on answer delay in patients with RESLES. We report a female patient who was admitted to our department for mixed aphasia accompanied by cognitive impairment. During the rapid improvement of aphasia, there was a clear phase of language output response delay accompanied by resolution of imaging lesions. We analyzed the course and the examination results of the patient and speculated the cause and pathogenesis. RESLES-relevant knowledge was systematically reviewed, which will help doctors in the classification of cerebral function and the diagnosis of RESLES. The specific language and cognitive impairment may be associated with the damage of contact fibers in the bilateral primary and secondary sensory and motor cortices.

The ascending reticular activating system (ARAS) is known to play an essential role in maintaining arousal and consciousness. In this report, we describe the case of a patient with impaired consciousness due to injury of the ARAS after bilateral pontine infarction. A 73-year-old female patient presented with anterior chest pain to the Emergency Department of our university hospital. She was diagnosed with chronic stable angina pectoris, three-vessel disease, and chronic total occlusion of the left anterior descending artery by coronary angiography and received conservative treatment. After five days, she showed deep drowsy mentality and brain MRI revealed bilateral paramedian pontine infarction. Four weeks after the pontine infarction, she showed severely impaired consciousness, with a Glasgow Coma Scale score of 7 (eye-opening: 2, best verbal response: 2, and best motor response: 3). Coma Recovery Scale-Revised score was 10 (auditory function: 2, visual function: 3, motor function: 2, verbal function: 2, communication: 0, and arousal: 1). Results of diffusion tensor tractography (DTT) for the ARAS showed decreased neural connectivity in the left lower dorsal ARAS, both lower ventral ARAS, and both upper ARAS. To the best of our knowledge, this is the first report of injury to the ARAS in bilateral pontine infarction diagnosed by DTT. We presume that our report would provide clinicians a better understanding of the mechanism of impaired consciousness in patients with pontine infarction.

Neuroglial cells have a high level of plasticity, and many types of these cells are present in the nervous system. Neuroglial cells provide diverse therapeutic targets for neurological diseases and injury repair. Cell reprogramming technology provides an efficient pathway for cell transformation during neural regeneration, while transcription factor-mediated reprogramming can facilitate the understanding of how neuroglial cells mature into functional neurons and promote neurological function recovery.

Most research has mainly focused on the decline of the subjective experience in Alzheimer’s disease (AD). However, few attempts have been made to evaluate whether subjective experience may be maintained in AD. In this narrative review, we attempt to provide a positive view, according to which patients with AD can enjoy, to some extent, subjective experience during memory retrieval. Memory and expression difficulties (e.g., aphasia) limit the ability of patients with AD to describe their memories, resulting in a little specificity of reported memories. However, according to the “authentic subjective experience” view, we propose in this study that the ability to mentally relive these memories could be preserved in the patients. By proposing the authentic subjective experience view, we attempt to provide an alternative view to the general consideration that the patients suffer a diminished subjective experience. This view can contribute to a larger clinical framework that gives a positive meaning to the subjective experience of patients with AD. Furthermore, several clinical and empirical implications can be drawn from the authentic subjective experience view, including the possibility to evaluate behavioral correlates of the subjective experience in AD.

The 2019 novel coronavirus pandemic, severe acute respiratory syndrome CoV-2 (COVID-19), has been a worldwide urgent public health threat, resulting in six-hundred seventy thousand deaths to date. The COVID-19 pandemic has led to a series of public health challenges. One such challenge is the management of diseases such as chronic neurological diseases during an epidemic event. COVID-19 affects all kinds of people, including older people with chronic underlying diseases, who are particularly at risk of severe infection or even death. Chronic neurological diseases such as epilepsy, dementia, Parkinson’s disease (PD), and multiple sclerosis (MS) are frequently associated with comorbidities; thus, these patients are in the high-risk category. Therefore, in this article, we review associations and challenges the people with epilepsy, dementia, PD, and MS faces during the COVID-19 pandemic and suggest approaches to provide consensus recommendations on how to provide the best possible care.

The present study was performed to evaluate the effects of ormosanine against spinal cord injury (SCI) in rats and to examine the possible molecular mechanism of action. SCI was induced using an impactor device, and rats were treated with ormosanine 10, 50 or 100 mg/kg, p.o., for 10 days after induction of SCI. The effect of ormosanine on SCI was determined by estimating neurological functions and cytokines and parameters of oxidative stress level were estimated in SCI rats. Quantitative reverse transcription polymerase chain reaction, Western blotting analysis and histopathological study were performed on spinal tissue of SCI rats. The data suggested that treatment with ormosanine reversed the alterations of neurological function in SCI rats. Moreover, the levels of cytokines, oxidative stress and reactive oxygen species production were reduced in the ormosanine treatment group compared to the SCI group. The levels of calpain and neuronal nitric oxide synthase activity were significantly reduced in the spinal tissue of the ormosanine treatment group compared to the SCI group. Moreover, ormosanine treatment reduced the percentage of viable neurons in the spinal tissue of SCI rats. In conclusion, the results of this study showed that ormosanine treatment had a protective effect against neuronal injury in spinal cord-injured rats by regulating the peroxynitrite/calpain activity.