Pub Date : 2022-07-16eCollection Date: 2022-01-01DOI: 10.1155/2022/6197505
Lucia Mencarelli, Lucia Monti, Sara Romanella, Francesco Neri, Giacomo Koch, Ricardo Salvador, Giulio Ruffini, Giulia Sprugnoli, Simone Rossi, Emiliano Santarnecchi
Over the past few years, the possibility of modulating fast brain oscillatory activity in the gamma (γ) band through transcranial alternating current stimulation (tACS) has been discussed in the context of both cognitive enhancement and therapeutic scenarios. However, the effects of tACS targeting regions outside the motor cortex, as well as its spatial specificity, are still unclear. Here, we present a concurrent tACS-fMRI block design study to characterize the impact of 40 Hz tACS applied over the left and right dorsolateral prefrontal cortex (DLPFC) in healthy subjects. Results suggest an increase in blood oxygenation level-dependent (BOLD) activity in the targeted bilateral DLPFCs, as well as in surrounding brain areas affected by stimulation according to biophysical modeling, i.e., the premotor cortex and anterior cingulate cortex (ACC). However, off-target effects were also observed, primarily involving the visual cortices, with further effects on the supplementary motor areas (SMA), left subgenual cingulate, and right superior temporal gyrus. The specificity of 40 Hz tACS over bilateral DLPFC and the possibility for network-level effects should be considered in future studies, especially in the context of recently promoted gamma-induction therapeutic protocols for neurodegenerative disorders.
{"title":"Local and Distributed fMRI Changes Induced by 40 Hz Gamma tACS of the Bilateral Dorsolateral Prefrontal Cortex: A Pilot Study.","authors":"Lucia Mencarelli, Lucia Monti, Sara Romanella, Francesco Neri, Giacomo Koch, Ricardo Salvador, Giulio Ruffini, Giulia Sprugnoli, Simone Rossi, Emiliano Santarnecchi","doi":"10.1155/2022/6197505","DOIUrl":"https://doi.org/10.1155/2022/6197505","url":null,"abstract":"<p><p>Over the past few years, the possibility of modulating fast brain oscillatory activity in the gamma (<i>γ</i>) band through transcranial alternating current stimulation (tACS) has been discussed in the context of both cognitive enhancement and therapeutic scenarios. However, the effects of tACS targeting regions outside the motor cortex, as well as its spatial specificity, are still unclear. Here, we present a concurrent tACS-fMRI block design study to characterize the impact of 40 Hz tACS applied over the left and right dorsolateral prefrontal cortex (DLPFC) in healthy subjects. Results suggest an increase in blood oxygenation level-dependent (BOLD) activity in the targeted bilateral DLPFCs, as well as in surrounding brain areas affected by stimulation according to biophysical modeling, i.e., the premotor cortex and anterior cingulate cortex (ACC). However, off-target effects were also observed, primarily involving the visual cortices, with further effects on the supplementary motor areas (SMA), left subgenual cingulate, and right superior temporal gyrus. The specificity of 40 Hz tACS over bilateral DLPFC and the possibility for network-level effects should be considered in future studies, especially in the context of recently promoted gamma-induction therapeutic protocols for neurodegenerative disorders.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":" ","pages":"6197505"},"PeriodicalIF":3.1,"publicationDate":"2022-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9308536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40539114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-07-13eCollection Date: 2022-01-01DOI: 10.1155/2022/7536783
Zicai Liu, Dongling Xie, Xin Wen, Risheng Wang, Quan Yang, Huiyu Liu, Yuchun Shao, Tingting Liu
Purpose: The purpose of this study was to evaluate the clinical efficacy of peripheral repetitive transcranial magnetic stimulation (rTMS) in the treatment of idiopathic facial paralysis, to explore an ideal treatment scheme for idiopathic facial paralysis, and to provide evidence for clinical rehabilitation.
Methods: 65 patients with idiopathic facial nerve palsy with the first onset were recruited and randomly divided into rTMS group and control group. Both groups received conventional treatment, rTMS group received additional repetitive transcranial magnetic stimulation to the affected side once a day, 5 times a week for 2 weeks. House-Brackmann (HB) grading scale, Sunnybrook facial grading system (SFGS), and modified Portmann scale (MPS) were used to assess facial nerve function before and after treatment, and the time for patients to return to normal facial nerve function and adverse reaction (AR) was also the main observation index.
Results: After a 2-week intervention, HB, SFGS, and MPS increased in both groups (P < 0.01); the improvement of HB, SFGS, and MPS in rTMS group was significantly higher than that in control group (P < 0.01). The effective improvement rate of the TMS group after 2 weeks was 90.0%, and that of the control group was 53.3%, and the difference was statistically significant (P < 0.01).
Conclusions: Repetitive transcranial magnetic stimulation is a safe and effective noninvasive method for the treatment of idiopathic facial paralysis, which can significantly accelerate the recovery of facial nerve function and provide a new treatment idea for further improving the prognosis of patients with idiopathic facial paralysis.
{"title":"Peripheral Repetitive Transcranial Magnetic Stimulation(rTMS) for Idiopathic Facial Nerve Palsy: A Prospective, Randomized Controlled Trial.","authors":"Zicai Liu, Dongling Xie, Xin Wen, Risheng Wang, Quan Yang, Huiyu Liu, Yuchun Shao, Tingting Liu","doi":"10.1155/2022/7536783","DOIUrl":"https://doi.org/10.1155/2022/7536783","url":null,"abstract":"<p><strong>Purpose: </strong>The purpose of this study was to evaluate the clinical efficacy of peripheral repetitive transcranial magnetic stimulation (rTMS) in the treatment of idiopathic facial paralysis, to explore an ideal treatment scheme for idiopathic facial paralysis, and to provide evidence for clinical rehabilitation.</p><p><strong>Methods: </strong>65 patients with idiopathic facial nerve palsy with the first onset were recruited and randomly divided into rTMS group and control group. Both groups received conventional treatment, rTMS group received additional repetitive transcranial magnetic stimulation to the affected side once a day, 5 times a week for 2 weeks. House-Brackmann (HB) grading scale, Sunnybrook facial grading system (SFGS), and modified Portmann scale (MPS) were used to assess facial nerve function before and after treatment, and the time for patients to return to normal facial nerve function and adverse reaction (AR) was also the main observation index.</p><p><strong>Results: </strong>After a 2-week intervention, HB, SFGS, and MPS increased in both groups (<i>P</i> < 0.01); the improvement of HB, SFGS, and MPS in rTMS group was significantly higher than that in control group (<i>P</i> < 0.01). The effective improvement rate of the TMS group after 2 weeks was 90.0%, and that of the control group was 53.3%, and the difference was statistically significant (<i>P</i> < 0.01).</p><p><strong>Conclusions: </strong>Repetitive transcranial magnetic stimulation is a safe and effective noninvasive method for the treatment of idiopathic facial paralysis, which can significantly accelerate the recovery of facial nerve function and provide a new treatment idea for further improving the prognosis of patients with idiopathic facial paralysis.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":" ","pages":"7536783"},"PeriodicalIF":3.1,"publicationDate":"2022-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9300274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40622973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Temporal lobe epilepsy (TLE) is a chronic neurological disorder that is often resistant to antiepileptic drugs. The pathogenesis of TLE is extremely complicated and remains elusive. Understanding the molecular mechanisms underlying TLE is crucial for its diagnosis and treatment. In the present study, a lithium-pilocarpine-induced TLE model was employed to reveal the pathological changes of hippocampus in rats. Hippocampal samples were taken for proteomic analysis at 2 weeks after the onset of spontaneous seizure (a chronic stage of epileptogenesis). Isobaric tag for relative and absolute quantization (iTRAQ) coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) technique was applied for proteomic analysis of hippocampus. A total of 4173 proteins were identified from the hippocampi of epileptic rats and its control, of which 27 differentially expressed proteins (DEPs) were obtained with a fold change > 1.5 and P < 0.05. Bioinformatics analysis indicated 27 DEPs were mainly enriched in "regulation of synaptic plasticity and structure" and "calmodulin-dependent protein kinase activity," which implicate synaptic remodeling may play a vital role in the pathogenesis of TLE. Consequently, the synaptic plasticity-related proteins and synaptic structure were investigated to verify it. It has been demonstrated that CaMKII-α, CaMKII-β, and GFAP were significant upregulated coincidently with proteomic analysis in the hippocampus of TLE rats. Moreover, the increased dendritic spines and hippocampal sclerosis further proved that synaptic plasticity involves in the development of TLE. The present study may help to understand the molecular mechanisms underlying epileptogenesis and provide a basis for further studies on synaptic plasticity in TLE.
{"title":"Proteomic Analysis Reveals the Vital Role of Synaptic Plasticity in the Pathogenesis of Temporal Lobe Epilepsy.","authors":"Xu Qian, Ji-Qiang Ding, Xin Zhao, Xin-Wen Sheng, Zhao-Rui Wang, Qi-Xing Yang, Jing-Jun Zheng, Jia-Gui Zhong, Teng-Yue Zhang, Shu-Qiao He, Wei-Dong Ji, Wei Li, Mei Zhang","doi":"10.1155/2022/8511066","DOIUrl":"https://doi.org/10.1155/2022/8511066","url":null,"abstract":"<p><p>Temporal lobe epilepsy (TLE) is a chronic neurological disorder that is often resistant to antiepileptic drugs. The pathogenesis of TLE is extremely complicated and remains elusive. Understanding the molecular mechanisms underlying TLE is crucial for its diagnosis and treatment. In the present study, a lithium-pilocarpine-induced TLE model was employed to reveal the pathological changes of hippocampus in rats. Hippocampal samples were taken for proteomic analysis at 2 weeks after the onset of spontaneous seizure (a chronic stage of epileptogenesis). Isobaric tag for relative and absolute quantization (iTRAQ) coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) technique was applied for proteomic analysis of hippocampus. A total of 4173 proteins were identified from the hippocampi of epileptic rats and its control, of which 27 differentially expressed proteins (DEPs) were obtained with a fold change > 1.5 and <i>P</i> < 0.05. Bioinformatics analysis indicated 27 DEPs were mainly enriched in \"regulation of synaptic plasticity and structure\" and \"calmodulin-dependent protein kinase activity,\" which implicate synaptic remodeling may play a vital role in the pathogenesis of TLE. Consequently, the synaptic plasticity-related proteins and synaptic structure were investigated to verify it. It has been demonstrated that CaMKII-<i>α</i>, CaMKII-<i>β</i>, and GFAP were significant upregulated coincidently with proteomic analysis in the hippocampus of TLE rats. Moreover, the increased dendritic spines and hippocampal sclerosis further proved that synaptic plasticity involves in the development of TLE. The present study may help to understand the molecular mechanisms underlying epileptogenesis and provide a basis for further studies on synaptic plasticity in TLE.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":" ","pages":"8511066"},"PeriodicalIF":3.1,"publicationDate":"2022-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9293557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40609498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-06-29eCollection Date: 2022-01-01DOI: 10.1155/2022/3300327
Kun Hou, Zhi-Cheng Xiao, Hai-Long Dai
Cerebral ischemia/reperfusion (I/R) injury is a complex pathophysiological process that can lead to neurological function damage and the formation of cerebral infarction. The p38 MAPK pathway has attracted considerable attention in cerebral I/R injury (IRI), but little research has been carried out on its direct role in vivo. In this study, to observe the effects of p38 MAPK endogenous inhibition on cerebral IRI, p38 heterozygous knockdown (p38KI/+) mice were used. We hypothesized that p38 signaling might be involved in I/R injury and neurological damage reduction and that neurological behavioral deficits improve when p38 MAPK is inhibited. First, we examined the neurological damage and neurological behavioral deficit effects of I/R injury in WT mice. Cerebral I/R injury was induced by the bilateral common carotid artery occlusion (BCCAO) method. The cerebral infarction area and volume were assessed and analyzed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. p38 MAPK and caspase-3 were detected by western blotting. Neuronal apoptosis was measured using TUNEL staining. Neurological deficits were detected by behavioral testing. Furthermore, to assess whether these neuroprotective effects occurred when p38 MAPK was inhibited, p38 heterozygous knockdown (p38KI/+) mice were used. We found that p38 MAPK endogenous inhibition rescued hippocampal cell apoptosis, reduced ischemic penumbra, and improved neurological behavioral deficits. These findings showed that p38 MAPK endogenous inhibition had a neuroprotective effect on IRI and that p38 MAPK may be a potential therapeutic target for cerebral IRI.
{"title":"p38 MAPK Endogenous Inhibition Improves Neurological Deficits in Global Cerebral Ischemia/Reperfusion Mice.","authors":"Kun Hou, Zhi-Cheng Xiao, Hai-Long Dai","doi":"10.1155/2022/3300327","DOIUrl":"https://doi.org/10.1155/2022/3300327","url":null,"abstract":"<p><p>Cerebral ischemia/reperfusion (I/R) injury is a complex pathophysiological process that can lead to neurological function damage and the formation of cerebral infarction. The p38 MAPK pathway has attracted considerable attention in cerebral I/R injury (IRI), but little research has been carried out on its direct role in vivo. In this study, to observe the effects of p38 MAPK endogenous inhibition on cerebral IRI, p38 heterozygous knockdown (p38<sup>KI/+</sup>) mice were used. We hypothesized that p38 signaling might be involved in I/R injury and neurological damage reduction and that neurological behavioral deficits improve when p38 MAPK is inhibited. First, we examined the neurological damage and neurological behavioral deficit effects of I/R injury in WT mice. Cerebral I/R injury was induced by the bilateral common carotid artery occlusion (BCCAO) method. The cerebral infarction area and volume were assessed and analyzed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. p38 MAPK and caspase-3 were detected by western blotting. Neuronal apoptosis was measured using TUNEL staining. Neurological deficits were detected by behavioral testing. Furthermore, to assess whether these neuroprotective effects occurred when p38 MAPK was inhibited, p38 heterozygous knockdown (p38<sup>KI/+</sup>) mice were used. We found that p38 MAPK endogenous inhibition rescued hippocampal cell apoptosis, reduced ischemic penumbra, and improved neurological behavioral deficits. These findings showed that p38 MAPK endogenous inhibition had a neuroprotective effect on IRI and that p38 MAPK may be a potential therapeutic target for cerebral IRI.</p>","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":" ","pages":"3300327"},"PeriodicalIF":3.1,"publicationDate":"2022-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9259354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40488502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jian-Min Chen, Qing-Fa Chen, Zhi-Yong Wang, Guo-Xin Ni
The electrophysiological recording can be used to quantify the clinical features of central poststroke pain (CPSP) caused by different lesion locations. We aimed to explore the relationship between clinical features and lesion location in patients with CPSP using the current perception threshold (CPT) approach. Here, patients underwent the standardized CPT measure at five detection sites on both the contralesional and ipsilesional sides, using a constant alternating-current sinusoid waveform stimulus at three frequencies: 2000 Hz, 250 Hz, and 5 Hz. 57 CPSP patients were recruited in this cross-sectional study, including 13 patients with thalamic lesions and 44 patients with internal capsule lesions. Patients with a thalamic lesion had more frequent abnormal Aδ and C fibers than those with an internal capsule lesion (69.2% versus 36.4%, p value = 0.038; 53.8% versus 63.6%, p value = 0.038). The patients with internal capsule lesions had more frequent abnormal Aβ fibers than those with thalamic lesions (53.8% versus 63.6%, p value < 0.001). The sensory dysfunction in the patients with thalamic lesions was more likely to occur in the upper limbs (i.e., the shoulder (p value = 0.027) and the finger (p value = 0.040)). The lower limbs (i.e., the knee (p value = 0.040) and the toe (p value = 0.005)) were more likely to experience sensory dysfunction in the patients with internal capsule lesions. Hyperesthesia was more likely to occur in the thalamic patients, and hypoesthesia was more likely to occur in the patients with internal capsule lesions (p value < 0.001). In patients with thalamic lesions, Visual Analogue Scale (VAS) had a positive correlation with 5 Hz CPT on the shoulder (r = 0.010, p value = 0.005), 250 Hz CPT on the finger (r = 0.690, p value = 0.009) from the contralesional side, and 2000 Hz CPT on the knee (r = 0.690, p value = 0.009). In patients with internal capsule lesions, VAS had a positive correlation with 2000 Hz CPT on the knee (r = 0.312, p value = 0.039) and foot (r = 0.538, p value < 0.001). In conclusion, the abnormal fiber types, sensory dysfunction territory, and clinical signs of CPSP in thalamic stroke differ from those in internal capsule stroke. Implementation of the portable and convenient CPT protocol may help clarify the locations of different stroke lesions in various clinical settings.
{"title":"Quantitative and Fiber-Selective Evaluation for Central Poststroke Pain","authors":"Jian-Min Chen, Qing-Fa Chen, Zhi-Yong Wang, Guo-Xin Ni","doi":"10.1155/2022/1507291","DOIUrl":"https://doi.org/10.1155/2022/1507291","url":null,"abstract":"The electrophysiological recording can be used to quantify the clinical features of central poststroke pain (CPSP) caused by different lesion locations. We aimed to explore the relationship between clinical features and lesion location in patients with CPSP using the current perception threshold (CPT) approach. Here, patients underwent the standardized CPT measure at five detection sites on both the contralesional and ipsilesional sides, using a constant alternating-current sinusoid waveform stimulus at three frequencies: 2000 Hz, 250 Hz, and 5 Hz. 57 CPSP patients were recruited in this cross-sectional study, including 13 patients with thalamic lesions and 44 patients with internal capsule lesions. Patients with a thalamic lesion had more frequent abnormal Aδ and C fibers than those with an internal capsule lesion (69.2% versus 36.4%, p value = 0.038; 53.8% versus 63.6%, p value = 0.038). The patients with internal capsule lesions had more frequent abnormal Aβ fibers than those with thalamic lesions (53.8% versus 63.6%, p value < 0.001). The sensory dysfunction in the patients with thalamic lesions was more likely to occur in the upper limbs (i.e., the shoulder (p value = 0.027) and the finger (p value = 0.040)). The lower limbs (i.e., the knee (p value = 0.040) and the toe (p value = 0.005)) were more likely to experience sensory dysfunction in the patients with internal capsule lesions. Hyperesthesia was more likely to occur in the thalamic patients, and hypoesthesia was more likely to occur in the patients with internal capsule lesions (p value < 0.001). In patients with thalamic lesions, Visual Analogue Scale (VAS) had a positive correlation with 5 Hz CPT on the shoulder (r = 0.010, p value = 0.005), 250 Hz CPT on the finger (r = 0.690, p value = 0.009) from the contralesional side, and 2000 Hz CPT on the knee (r = 0.690, p value = 0.009). In patients with internal capsule lesions, VAS had a positive correlation with 2000 Hz CPT on the knee (r = 0.312, p value = 0.039) and foot (r = 0.538, p value < 0.001). In conclusion, the abnormal fiber types, sensory dysfunction territory, and clinical signs of CPSP in thalamic stroke differ from those in internal capsule stroke. Implementation of the portable and convenient CPT protocol may help clarify the locations of different stroke lesions in various clinical settings.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"16 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87372828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jingyan Tao, Zhaoqing Li, Yang Liu, Jianhua Li, Ruiliang Bai
Several neuroimaging methods have been proposed to assess the integrity of the corticospinal tract (CST) for predicting recovery of motor function after stroke, including conventional structural magnetic resonance imaging (sMRI) and diffusion tensor imaging (DTI). In this study, we aimed to compare the predicative performance of these methods using different neuroimaging modalities and optimize the prediction protocol for upper limb motor function after stroke in a clinical environment. We assessed 28 first-ever stroke patients with upper limb motor impairment. We used the upper extremity module of the Fugl-Meyer assessment (UE-FM) within 1 month of onset (baseline) and again 3 months poststroke. sMRI (T1- and T2-based) was used to measure CST-weighted lesion load (CST-wLL), and DTI was used to measure the fractional anisotropy asymmetry index (FAAI) and the ratio of fractional anisotropy (rFA). The CST-wLL within 1 month poststroke was closely correlated with upper limb motor outcomes and recovery potential. CST‐wLL ≥ 2.068 cc indicated serious CST damage and a poor outcome (100%). CST‐wLL < 1.799 cc was correlated with a considerable rate (>70%) of upper limb motor function recovery. CST-wLL showed a comparable area under the curve (AUC) to that of the CST-FAAI (p = 0.71). Inclusion of extra-CST-FAAI did not significantly increase the AUC (p = 0.58). Our findings suggest that sMRI-derived CST-wLL is a precise predictor of upper limb motor outcomes 3 months poststroke. We recommend this parameter as a predictive imaging biomarker for classifying patients' recovery prognosis in clinical practice. Conversely, including DTI appeared to induce no significant benefits.
{"title":"Performance Comparison of Different Neuroimaging Methods for Predicting Upper Limb Motor Outcomes in Patients after Stroke","authors":"Jingyan Tao, Zhaoqing Li, Yang Liu, Jianhua Li, Ruiliang Bai","doi":"10.1155/2022/4203698","DOIUrl":"https://doi.org/10.1155/2022/4203698","url":null,"abstract":"Several neuroimaging methods have been proposed to assess the integrity of the corticospinal tract (CST) for predicting recovery of motor function after stroke, including conventional structural magnetic resonance imaging (sMRI) and diffusion tensor imaging (DTI). In this study, we aimed to compare the predicative performance of these methods using different neuroimaging modalities and optimize the prediction protocol for upper limb motor function after stroke in a clinical environment. We assessed 28 first-ever stroke patients with upper limb motor impairment. We used the upper extremity module of the Fugl-Meyer assessment (UE-FM) within 1 month of onset (baseline) and again 3 months poststroke. sMRI (T1- and T2-based) was used to measure CST-weighted lesion load (CST-wLL), and DTI was used to measure the fractional anisotropy asymmetry index (FAAI) and the ratio of fractional anisotropy (rFA). The CST-wLL within 1 month poststroke was closely correlated with upper limb motor outcomes and recovery potential. CST‐wLL ≥ 2.068 cc indicated serious CST damage and a poor outcome (100%). CST‐wLL < 1.799 cc was correlated with a considerable rate (>70%) of upper limb motor function recovery. CST-wLL showed a comparable area under the curve (AUC) to that of the CST-FAAI (p = 0.71). Inclusion of extra-CST-FAAI did not significantly increase the AUC (p = 0.58). Our findings suggest that sMRI-derived CST-wLL is a precise predictor of upper limb motor outcomes 3 months poststroke. We recommend this parameter as a predictive imaging biomarker for classifying patients' recovery prognosis in clinical practice. Conversely, including DTI appeared to induce no significant benefits.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"52 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74944617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Tian, Zeyu Wang, Yadi Ren, Yong Jiang, Ying Zhao, Man Li, Zhiguang Zhang
Background Helicobacter pylori (H. pylori) infection is closely associated with depression and development of neuroinflammation. The aim of this study is to explore the relationship between H. pylori, depression, and circulating levels of ghrelin. Methods Mice were randomly divided into three groups: healthy control group (gavaged sterile saline and injected with saline, n = 8); H. pylori+saline group (gavaged H. pylori and injected with saline, n = 8); and H. pylori+rapa group (gavaged H. pylori and injected with rapamycin, n = 8). Open field test (OFT), sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST) were used for anxiety and depressive behavior test. Western blotting was utilized to assess mTOR, p-mTOR, and GSMD expression, and serum ghrelin levels were estimated using ELISA. Results In the OFT, the control mice moved more and exhibited a increase in crossing number relative to the H. pylori+saline mice (all P < 0.05). Increased quantity of fecal boli can be indicative of increased anxiety and emotionality of the subject animal. H. pylori+saline mice exhibited an increase in fecal boli when compared to control mice and H. pylori+rapa mice (P < 0.05). H. pylori infected mice decreasing the expression of ghrelin. The protein levels of p-mTOR/mTOR in the gastric antrum mTOR signaling activation and low-level ghrelin in H. pylori-infect mice compared to those in control mice (all P <0.001). Compared with single H. pylori infection, mTOR inhibitors increased the ghrelin secretion of H. pylori infection to a certain extent (P < 0.05). The protein levels of GSDMD expression significantly increase in hippocampus of H. pylori-infected mice (P < 0.001). Rapamycin treatment inhibited expression of GSDMD in H. pylori-infected mice (P < 0.05). Conclusions H. pylori infection is associated with increased expression of mTOR and decreased circulating levels of ghrelin. Elevated pyroptosis in the brain and anxiety- and depressed-like behaviors occur when ghrelin levels are suppressed.
{"title":"Rapamycin Attenuates Anxiety and Depressive Behavior Induced by Helicobacter pylori in Association with Reduced Circulating Levels of Ghrelin","authors":"J. Tian, Zeyu Wang, Yadi Ren, Yong Jiang, Ying Zhao, Man Li, Zhiguang Zhang","doi":"10.1155/2022/2847672","DOIUrl":"https://doi.org/10.1155/2022/2847672","url":null,"abstract":"Background Helicobacter pylori (H. pylori) infection is closely associated with depression and development of neuroinflammation. The aim of this study is to explore the relationship between H. pylori, depression, and circulating levels of ghrelin. Methods Mice were randomly divided into three groups: healthy control group (gavaged sterile saline and injected with saline, n = 8); H. pylori+saline group (gavaged H. pylori and injected with saline, n = 8); and H. pylori+rapa group (gavaged H. pylori and injected with rapamycin, n = 8). Open field test (OFT), sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST) were used for anxiety and depressive behavior test. Western blotting was utilized to assess mTOR, p-mTOR, and GSMD expression, and serum ghrelin levels were estimated using ELISA. Results In the OFT, the control mice moved more and exhibited a increase in crossing number relative to the H. pylori+saline mice (all P < 0.05). Increased quantity of fecal boli can be indicative of increased anxiety and emotionality of the subject animal. H. pylori+saline mice exhibited an increase in fecal boli when compared to control mice and H. pylori+rapa mice (P < 0.05). H. pylori infected mice decreasing the expression of ghrelin. The protein levels of p-mTOR/mTOR in the gastric antrum mTOR signaling activation and low-level ghrelin in H. pylori-infect mice compared to those in control mice (all P <0.001). Compared with single H. pylori infection, mTOR inhibitors increased the ghrelin secretion of H. pylori infection to a certain extent (P < 0.05). The protein levels of GSDMD expression significantly increase in hippocampus of H. pylori-infected mice (P < 0.001). Rapamycin treatment inhibited expression of GSDMD in H. pylori-infected mice (P < 0.05). Conclusions H. pylori infection is associated with increased expression of mTOR and decreased circulating levels of ghrelin. Elevated pyroptosis in the brain and anxiety- and depressed-like behaviors occur when ghrelin levels are suppressed.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"42 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81143675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Accurate motor timing requires the temporally precise coupling between sensory input and motor output including the adjustment of movements with respect to changes in the environment. Such error correction has been related to a cerebello-thalamo-cortical network. At least partially distinct networks for the correction of perceived (i.e., conscious) as compared to nonperceived (i.e., nonconscious) errors have been suggested. While the cerebellum, the premotor, and the prefrontal cortex seem to be involved in conscious error correction, the network subserving nonconscious error correction is less clear. The present study is aimed at investigating the functional contribution of the primary motor cortex (M1) for both types of error correction in the temporal domain. To this end, anodal transcranial direct current stimulation (atDCS) was applied to the left M1 in a group of 18 healthy young volunteers during a resting period of 10 minutes. Sensorimotor synchronization as well as error correction of the right index finger was tested immediately prior to and after atDCS. Sham stimulation served as control condition. To induce error correction, nonconscious and conscious temporal step-changes were interspersed in a sequence of an isochronous auditory pacing signal in either direction (i.e., negative or positive) yielding either shorter or longer intervals. Prior to atDCS, faster error correction in conscious as compared to nonconscious trials was observed replicating previous findings. atDCS facilitated nonconscious error correction, but only in trials with negative step-changes yielding shorter intervals. In contrast to this, neither tapping speed nor synchronization performance with respect to the isochronous pacing signal was significantly modulated by atDCS. The data suggest M1 as part of a network distinctively contributing to the correction of nonconscious negative step-changes going beyond sensorimotor synchronization.
{"title":"Anodal Transcranial Direct Current Stimulation (atDCS) of the Primary Motor Cortex (M1) Facilitates Nonconscious Error Correction of Negative Phase Shifts","authors":"B. Pollok, Martin Jurkiewicz, V. Krause","doi":"10.1155/2022/9419154","DOIUrl":"https://doi.org/10.1155/2022/9419154","url":null,"abstract":"Accurate motor timing requires the temporally precise coupling between sensory input and motor output including the adjustment of movements with respect to changes in the environment. Such error correction has been related to a cerebello-thalamo-cortical network. At least partially distinct networks for the correction of perceived (i.e., conscious) as compared to nonperceived (i.e., nonconscious) errors have been suggested. While the cerebellum, the premotor, and the prefrontal cortex seem to be involved in conscious error correction, the network subserving nonconscious error correction is less clear. The present study is aimed at investigating the functional contribution of the primary motor cortex (M1) for both types of error correction in the temporal domain. To this end, anodal transcranial direct current stimulation (atDCS) was applied to the left M1 in a group of 18 healthy young volunteers during a resting period of 10 minutes. Sensorimotor synchronization as well as error correction of the right index finger was tested immediately prior to and after atDCS. Sham stimulation served as control condition. To induce error correction, nonconscious and conscious temporal step-changes were interspersed in a sequence of an isochronous auditory pacing signal in either direction (i.e., negative or positive) yielding either shorter or longer intervals. Prior to atDCS, faster error correction in conscious as compared to nonconscious trials was observed replicating previous findings. atDCS facilitated nonconscious error correction, but only in trials with negative step-changes yielding shorter intervals. In contrast to this, neither tapping speed nor synchronization performance with respect to the isochronous pacing signal was significantly modulated by atDCS. The data suggest M1 as part of a network distinctively contributing to the correction of nonconscious negative step-changes going beyond sensorimotor synchronization.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"30 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83341136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lumbar disc herniation (LDH) induced nerve compression syndromes have been a prevalent problem with complex neural mechanisms. Changes in distributed brain areas are involved in the occurrence and persistence of syndromes. The present study aimed to investigate the changes of brain functional network in LDH patients with chronic sciatica using graph theory analysis. A total of thirty LDH adults presenting L4 and/or L5 root (s) compression syndromes (LDH group) and thirty age-, sex-, BMI- and education-matched healthy control (HC group) were recruited for functional MRI scan. Whole-brain functional network was constructed for each participant using Pearson's correlation. Global and nodal properties were calculated and compared between two groups, including small-worldness index, clustering coefficient, characteristic path length, degree centrality (DC), betweenness centrality (BC) and nodal efficiency. Both LDH and HC groups showed small-world architecture in the functional network of brain. However, LDH group showed that nodal centralities (DC, BC and nodal efficiency) increased in opercular part of inferior frontal gyrus; and decreased in orbital part of inferior frontal gyrus, lingual cortex and inferior occipital gyrus. The DC and efficiency in the right inferior occipital gyrus were negatively related with the Oswestry Disability Index in LDH group. In conclusion, the LDH-related chronic sciatica syndromes may induce regional brain alterations involving self-referential, emotional responses and pain regulation functions. But the whole-brain small-world architecture was not significantly disturbed. It may provide new insights into LDH patients with radicular symptoms from new perspectives.
{"title":"Brain Network Changes in Lumbar Disc Herniation Induced Chronic Nerve Roots Compression Syndromes","authors":"Yan-Peng Zhang, Guang-Hui Hong, Chuan-Yin Zhang","doi":"10.1155/2022/7912410","DOIUrl":"https://doi.org/10.1155/2022/7912410","url":null,"abstract":"Lumbar disc herniation (LDH) induced nerve compression syndromes have been a prevalent problem with complex neural mechanisms. Changes in distributed brain areas are involved in the occurrence and persistence of syndromes. The present study aimed to investigate the changes of brain functional network in LDH patients with chronic sciatica using graph theory analysis. A total of thirty LDH adults presenting L4 and/or L5 root (s) compression syndromes (LDH group) and thirty age-, sex-, BMI- and education-matched healthy control (HC group) were recruited for functional MRI scan. Whole-brain functional network was constructed for each participant using Pearson's correlation. Global and nodal properties were calculated and compared between two groups, including small-worldness index, clustering coefficient, characteristic path length, degree centrality (DC), betweenness centrality (BC) and nodal efficiency. Both LDH and HC groups showed small-world architecture in the functional network of brain. However, LDH group showed that nodal centralities (DC, BC and nodal efficiency) increased in opercular part of inferior frontal gyrus; and decreased in orbital part of inferior frontal gyrus, lingual cortex and inferior occipital gyrus. The DC and efficiency in the right inferior occipital gyrus were negatively related with the Oswestry Disability Index in LDH group. In conclusion, the LDH-related chronic sciatica syndromes may induce regional brain alterations involving self-referential, emotional responses and pain regulation functions. But the whole-brain small-world architecture was not significantly disturbed. It may provide new insights into LDH patients with radicular symptoms from new perspectives.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"58 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73823519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A mounting body of evidence suggests that prenatal inflammation may enhance the rate of age-associated cognitive decline and may involve aberrant amounts of synaptic proteins in the hippocampus, including synaptotagmin-1 (Syt1) and activity-regulated cytoskeleton-associated protein (Arc). However, little is known about the specific impact of adolescent environmental enrichment (EE) on age-associated cognitive decline and the changes in synaptic proteins caused by prenatal inflammation. In this study, CD-1 mice in late pregnancy were given intraperitoneal doses of lipopolysaccharide (LPS, 50 μg/kg) or normal saline. Offspring arising from LPS dams were divided into a LPS group and a LPS plus EE (LPS-E) group. The LPS-E mice were exposed to EE from 2 months of age until the end of the experiment (3 or 15 months old). The Morris water maze (MWM) was used to assess the spatial learning and memory capacities of experimental mice, while western blotting and RNA-scope were used to determine the expression levels of Arc and Syt1 in the hippocampus at the protein and mRNA levels, respectively. Analysis revealed that at 15 months of age, the control mice experienced a reduction in cognitive ability and elevated expression levels of Arc and Syt1 genes when compared to control mice at 3 months of age. The LPS-E group exhibited better cognition and lower protein and mRNA levels of Arc and Syt1 than mice in the LPS group of the same age. However, the enriched environment mitigated but did not counteract, the effects of prenatal inflammation on cognitive and synaptic proteins when tested at either 3 or 15 months of age. Our findings revealed that long-term environmental enrichment improved the expression levels of synaptic proteins in CD-1 mice and that this effect was linked to the dysfunctional cognition caused by prenatal inflammation; this process may also be involved in the reduction of hippocampal Arc and Syt1 gene expression.
越来越多的证据表明，产前炎症可能会增加与年龄相关的认知能力下降的速度，并可能涉及海马中突触蛋白的异常数量，包括突触蛋白-1 (Syt1)和活动调节的细胞骨架相关蛋白(Arc)。然而，青少年环境富集(EE)对年龄相关认知能力下降和产前炎症引起的突触蛋白变化的具体影响知之甚少。在本研究中，CD-1孕晚期小鼠腹腔注射50 μg/kg的脂多糖(LPS)或生理盐水。将LPS母鼠分为LPS组和LPS + EE (LPS- e)组。LPS-E小鼠从2个月大开始暴露于EE，直到实验结束(3或15个月大)。采用Morris水迷宫(Morris water maze, MWM)评估实验小鼠的空间学习和记忆能力，采用western blotting和RNA-scope分别在蛋白和mRNA水平上检测Arc和Syt1在海马中的表达水平。分析显示，与3个月大的对照组小鼠相比，在15个月大时，对照小鼠的认知能力下降，Arc和Syt1基因的表达水平升高。与同龄LPS组相比，LPS- e组小鼠认知能力增强，Arc和Syt1蛋白及mRNA水平降低。然而，当在3个月或15个月大的时候测试时，丰富的环境减轻了但没有抵消产前炎症对认知和突触蛋白的影响。我们的研究结果表明，长期的环境富集改善了CD-1小鼠突触蛋白的表达水平，这种影响与产前炎症引起的认知功能障碍有关;这一过程也可能与海马Arc和Syt1基因表达的减少有关。
{"title":"Long-Term Environmental Enrichment Relieves Dysfunctional Cognition and Synaptic Protein Levels Induced by Prenatal Inflammation in Older CD-1 Mice","authors":"Zhe-Zhe Zhang, Li-ping Zeng, Jing Chen, Yong-Fang Wu, Ya-Tao Wang, Lan Xia, Qi-Gang Yang, Fang Wang, Gui-Hai Chen","doi":"10.1155/2022/1483101","DOIUrl":"https://doi.org/10.1155/2022/1483101","url":null,"abstract":"A mounting body of evidence suggests that prenatal inflammation may enhance the rate of age-associated cognitive decline and may involve aberrant amounts of synaptic proteins in the hippocampus, including synaptotagmin-1 (Syt1) and activity-regulated cytoskeleton-associated protein (Arc). However, little is known about the specific impact of adolescent environmental enrichment (EE) on age-associated cognitive decline and the changes in synaptic proteins caused by prenatal inflammation. In this study, CD-1 mice in late pregnancy were given intraperitoneal doses of lipopolysaccharide (LPS, 50 μg/kg) or normal saline. Offspring arising from LPS dams were divided into a LPS group and a LPS plus EE (LPS-E) group. The LPS-E mice were exposed to EE from 2 months of age until the end of the experiment (3 or 15 months old). The Morris water maze (MWM) was used to assess the spatial learning and memory capacities of experimental mice, while western blotting and RNA-scope were used to determine the expression levels of Arc and Syt1 in the hippocampus at the protein and mRNA levels, respectively. Analysis revealed that at 15 months of age, the control mice experienced a reduction in cognitive ability and elevated expression levels of Arc and Syt1 genes when compared to control mice at 3 months of age. The LPS-E group exhibited better cognition and lower protein and mRNA levels of Arc and Syt1 than mice in the LPS group of the same age. However, the enriched environment mitigated but did not counteract, the effects of prenatal inflammation on cognitive and synaptic proteins when tested at either 3 or 15 months of age. Our findings revealed that long-term environmental enrichment improved the expression levels of synaptic proteins in CD-1 mice and that this effect was linked to the dysfunctional cognition caused by prenatal inflammation; this process may also be involved in the reduction of hippocampal Arc and Syt1 gene expression.","PeriodicalId":19122,"journal":{"name":"Neural Plasticity","volume":"9 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2022-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90407106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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