Introduction: Postherpetic neuralgia (PHN) is one of the common refractory neuropathic pains. Oral drug treatment has great side effects and poor efficacy. To study the efficacy of computed tomography (CT)-guided pulsed radiofrequency (PRF) targeting dorsal root ganglion (DRG) and platelet-rich plasma (PRP), this retrospective observation was performed.
Material and methods: All patients with PHN were divided into the control group, PRF group, and PRF + PRP group based on their different treatment methods. The control group (45 cases) received drug treatment, the PRF group (45 cases) received CT-guided PRF treatment targeted to DRG, and the PRF + PRP group received PRF and PRP treatment. The changes of the numeric rating scale (NRS), Pittsburgh sleep quality index (PSQI) levels, and short form 36 health survey questionnaire (SF-36) before treatment and 7 days, 14 days, 30 days, and 90 days after treatment were compared among three groups.
Results: NRS and PSQI scores in the PRF + PRP group were lower than those in the PRF group and control group at 90 days after treatment ( p < 0.001). At 90 days after the operation, the scores of SF-36 in the PRF + PRP group were obviously elevated compared with the data of the control group and PRF group ( p < 0.001).
Conclusions: The pain degree, quality of sleep of patients, and quality of life with PHN were significantly improved after PRF combined with PRP treatments.
{"title":"Therapeutic effect of computed tomography-guided dorsal root ganglion pulsed radiofrequency regulation combined with platelet-rich plasma injection on postherpetic neuralgia: A retrospective study.","authors":"Zhongwei Wang, Jing Chen, Xiaona Guo, Yan Lin, Weipeng Ge, Yunchao Chu","doi":"10.5114/fn.2024.136436","DOIUrl":"https://doi.org/10.5114/fn.2024.136436","url":null,"abstract":"<p><strong>Introduction: </strong>Postherpetic neuralgia (PHN) is one of the common refractory neuropathic pains. Oral drug treatment has great side effects and poor efficacy. To study the efficacy of computed tomography (CT)-guided pulsed radiofrequency (PRF) targeting dorsal root ganglion (DRG) and platelet-rich plasma (PRP), this retrospective observation was performed.</p><p><strong>Material and methods: </strong>All patients with PHN were divided into the control group, PRF group, and PRF + PRP group based on their different treatment methods. The control group (45 cases) received drug treatment, the PRF group (45 cases) received CT-guided PRF treatment targeted to DRG, and the PRF + PRP group received PRF and PRP treatment. The changes of the numeric rating scale (NRS), Pittsburgh sleep quality index (PSQI) levels, and short form 36 health survey questionnaire (SF-36) before treatment and 7 days, 14 days, 30 days, and 90 days after treatment were compared among three groups.</p><p><strong>Results: </strong>NRS and PSQI scores in the PRF + PRP group were lower than those in the PRF group and control group at 90 days after treatment ( p < 0.001). At 90 days after the operation, the scores of SF-36 in the PRF + PRP group were obviously elevated compared with the data of the control group and PRF group ( p < 0.001).</p><p><strong>Conclusions: </strong>The pain degree, quality of sleep of patients, and quality of life with PHN were significantly improved after PRF combined with PRP treatments.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008509","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}
Introduction: There remains uncertainty about the mechanism and specific location of the relative cortex with nonketotic hyperglycaemic hemichorea-hemiballismus (HC-HB). This paper aims to analyse the relationship between the disappearance of HC-HB and the supplementary motor area (SMA) infarction in a patient who recovered following an acute ischemic stroke.
Case presentation: An 83-year-old female patient with diabetes mellitus presenting with severe and refractory involuntary movement after hypoglycaemic therapy was referred to an outpatient neurosurgery department for further intervention. Laboratory, magnetic resonance imaging (MRI) and computed tomography (CT) neuroimaging and physical examinations were performed. After a diagnosis of HC-HB was confirmed, the patient received hypoglycaemic therapy and haloperidol; however, there was no significant improvement. Brain MRI T1-weighted images and CT scans showed high signal intensity involving the bilateral putamen nucleus. CT perfusion and CT angiography showed a hypo-perfusion in the SMA of the right hemisphere without significant vascular occlusion. Then, aspirin and clopidogrel were administered, and the patient's left leg presented slight involuntary movement three days later. Interestingly, her involuntary movement disappeared again on the second day after the discontinuation of antiplatelet therapy. She was discharged three days later, and her symptoms did not recur during a follow-up for three months.
Conclusions: The SMA dysfunction caused by the acute infarction could terminate or reset the pathological neural path-way of nonketotic hyperglycaemic HC-HB and contribute to the disappearance of the involuntary movement on the contralateral side. The SMA may be a selective intervention target for patients with refractory nonketotic hyperglycaemic HC-HB.
{"title":"Recovery of nonketotic hyperglycaemic hemichorea -hemiballismus due to acute ischemic stroke in the contralateral supplementary motor area: a case report and literature review.","authors":"Xiuyu Du, Xiaochuan Guo, Xiaobao Zhou","doi":"10.5114/fn.2024.135290","DOIUrl":"https://doi.org/10.5114/fn.2024.135290","url":null,"abstract":"<p><strong>Introduction: </strong>There remains uncertainty about the mechanism and specific location of the relative cortex with nonketotic hyperglycaemic hemichorea-hemiballismus (HC-HB). This paper aims to analyse the relationship between the disappearance of HC-HB and the supplementary motor area (SMA) infarction in a patient who recovered following an acute ischemic stroke.</p><p><strong>Case presentation: </strong>An 83-year-old female patient with diabetes mellitus presenting with severe and refractory involuntary movement after hypoglycaemic therapy was referred to an outpatient neurosurgery department for further intervention. Laboratory, magnetic resonance imaging (MRI) and computed tomography (CT) neuroimaging and physical examinations were performed. After a diagnosis of HC-HB was confirmed, the patient received hypoglycaemic therapy and haloperidol; however, there was no significant improvement. Brain MRI T1-weighted images and CT scans showed high signal intensity involving the bilateral putamen nucleus. CT perfusion and CT angiography showed a hypo-perfusion in the SMA of the right hemisphere without significant vascular occlusion. Then, aspirin and clopidogrel were administered, and the patient's left leg presented slight involuntary movement three days later. Interestingly, her involuntary movement disappeared again on the second day after the discontinuation of antiplatelet therapy. She was discharged three days later, and her symptoms did not recur during a follow-up for three months.</p><p><strong>Conclusions: </strong>The SMA dysfunction caused by the acute infarction could terminate or reset the pathological neural path-way of nonketotic hyperglycaemic HC-HB and contribute to the disappearance of the involuntary movement on the contralateral side. The SMA may be a selective intervention target for patients with refractory nonketotic hyperglycaemic HC-HB.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008507","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}
Introduction: There has been an increasing trend in spinal surgery interventions in recent years. Low back pain is a disorder that is seen at least once in the lifetime of approximately 80% of the general population. Today, neurosurgeons perform operations including laminectomy for various reasons. Epidural fibrosis is a scar tissue that develops after posterior spinal surgery. Various synthetic and organic materials have been used in experimental studies to prevent epidural fibrosis in laminectomy defects. In this study we aimed to investigate and observe histopathologically the effectiveness of cyclooxygenase inhibitor drugs; tenoxicam and diclofenac sodium in the experimental rat laminectomy model in preventing the postoperative spinal epidural fibrosis.
Material and methods: In this study, 32 Wistar-Albino female rats were used. 8 mg/kg tenoxicam and 1.5 mg/kg diclofenac sodium were applied on the dura with an absorbable gelatin sponge. After decapitation, L1-L4 laminectomy area was totally removed and histopathological examination was performed.
Results and conclusions: It has been shown that the topical application of diclofenac sodium and tenoxicam, which are selective Cox inhibitor drugs, prevents fibroblast migration by forming a local barrier and Cox inhibitors are caused by the inhibition of prostanoids, which are inflammatory mediators.
{"title":"Comparison of the effectiveness of diclofenac sodium and tenoxicam in the prevention of epidural fibrosis by topical application with an absorbable gelatin sponge on the dura in an experimental laminectomy model.","authors":"Sule Gokturk, Yasin Gokturk, Suat Erol Celik","doi":"10.5114/fn.2024.141373","DOIUrl":"https://doi.org/10.5114/fn.2024.141373","url":null,"abstract":"<p><strong>Introduction: </strong>There has been an increasing trend in spinal surgery interventions in recent years. Low back pain is a disorder that is seen at least once in the lifetime of approximately 80% of the general population. Today, neurosurgeons perform operations including laminectomy for various reasons. Epidural fibrosis is a scar tissue that develops after posterior spinal surgery. Various synthetic and organic materials have been used in experimental studies to prevent epidural fibrosis in laminectomy defects. In this study we aimed to investigate and observe histopathologically the effectiveness of cyclooxygenase inhibitor drugs; tenoxicam and diclofenac sodium in the experimental rat laminectomy model in preventing the postoperative spinal epidural fibrosis.</p><p><strong>Material and methods: </strong>In this study, 32 Wistar-Albino female rats were used. 8 mg/kg tenoxicam and 1.5 mg/kg diclofenac sodium were applied on the dura with an absorbable gelatin sponge. After decapitation, L1-L4 laminectomy area was totally removed and histopathological examination was performed.</p><p><strong>Results and conclusions: </strong>It has been shown that the topical application of diclofenac sodium and tenoxicam, which are selective Cox inhibitor drugs, prevents fibroblast migration by forming a local barrier and Cox inhibitors are caused by the inhibition of prostanoids, which are inflammatory mediators.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008574","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}
Smilja Todorovic, Katarina Milosevic, Ana Milosevic, Marija M Janjic, Srdjan J Sokanovic, Danijela Savic, Irena Lavrnja
Dysregulations in cholesterol homeostasis contribute to the pathogenesis of multiple sclerosis (MS) and its best described animal model, experimental autoimmune encephalomyelitis (EAE). Cholesterol is an important component of myelin, which is necessary for signal transmission between neurons. Demyelination leads to the formation of oxysterols, degradation products of cholesterol that are ligands for nuclear liver X receptors (LXRs). Genes regulated by LXRs are involved in cholesterol efflux, absorption, transport, and excretion, which we investigated in this study. In this study, we detected changes in gene expression of Srebf1, Ldlr, Soat1, Abca1, Lrp1, and Npc1, all of which are important in the regulation of cholesterol homeostasis, during the course of EAE in male and female rats. In particular, differential expression of Srebf1, Ldlr, and Soat1 was observed in the spinal cord of male and female rats during EAE. Moreover, these genes are altered during EAE. In contrast, the expression of Abca1 and Lrp1 was significantly affected only by sex. In male animals, the expression of Npc1 is conspicuously reduced in EAE pathology. Thus, our study confirms the involvement of enzymes of cholesterol metabolism in the pathophysiology of EAE, with sex and disease progression affecting the expression of these genes. These findings may improve the understanding of neurodegenerative diseases associated with impaired lipid metabolism in the brain, such as MS/EAE.
{"title":"Expression of components involved in cholesterol homeostasis maintenance during experimental autoimmune encephalomyelitis in rat spinal cord.","authors":"Smilja Todorovic, Katarina Milosevic, Ana Milosevic, Marija M Janjic, Srdjan J Sokanovic, Danijela Savic, Irena Lavrnja","doi":"10.5114/fn.2024.141376","DOIUrl":"https://doi.org/10.5114/fn.2024.141376","url":null,"abstract":"<p><p>Dysregulations in cholesterol homeostasis contribute to the pathogenesis of multiple sclerosis (MS) and its best described animal model, experimental autoimmune encephalomyelitis (EAE). Cholesterol is an important component of myelin, which is necessary for signal transmission between neurons. Demyelination leads to the formation of oxysterols, degradation products of cholesterol that are ligands for nuclear liver X receptors (LXRs). Genes regulated by LXRs are involved in cholesterol efflux, absorption, transport, and excretion, which we investigated in this study. In this study, we detected changes in gene expression of Srebf1, Ldlr, Soat1, Abca1, Lrp1, and Npc1, all of which are important in the regulation of cholesterol homeostasis, during the course of EAE in male and female rats. In particular, differential expression of Srebf1, Ldlr, and Soat1 was observed in the spinal cord of male and female rats during EAE. Moreover, these genes are altered during EAE. In contrast, the expression of Abca1 and Lrp1 was significantly affected only by sex. In male animals, the expression of Npc1 is conspicuously reduced in EAE pathology. Thus, our study confirms the involvement of enzymes of cholesterol metabolism in the pathophysiology of EAE, with sex and disease progression affecting the expression of these genes. These findings may improve the understanding of neurodegenerative diseases associated with impaired lipid metabolism in the brain, such as MS/EAE.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008577","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}
Introduction: The present research focused on the function of lncRNA taurine upregulated 1 (TUG1) in a rat neuropathic pain (NP) model constructed by chronic contractile injury (CCI).
Material and methods: Construction of the NP rat model was performed by CCI surgery. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were applied to examine the NP behavior. RT-qPCR was established to explore the levels of TUG1, microRNA (miR)-29b-3p, and HMGB1. ELISA was carried out to evaluate the concentrations of interleukin (IL)-6, IL-1β, tumor necrosis factor α (TNF-α), IL-4, and IL-6. The underlying mechanisms of TUG1 were explored by RNA-binding protein immunoprecipitation (RIP) and dual-luciferase reporter (DLR) assay.
Results: TUG1 and HMGB1 were statistically elevated in the tissue of CCI rats, while miR-29b-3p was reduced. TUG1 competitively binds to miR-29b-3p to upregulate HMGB1 levels. Suppression of TUG1 persistently decreased PWL and PWT along with increased frequency of paw-lifting, whereas this alleviation was typically rescued by the abrogated miR-29b-3p. Analogously, knockdown of TUG1 inhibited CCI-induced overproduction of IL-6, IL-1β, and TNF-α, and reduction of IL-4 and IL-6, but this inhibition was partially abrogated by the reduction of miR-29b-3p.
Conclusions: Suppression TUG1 can alleviate NP hypersensitivity and neuroinflammation in CCI rats by competitively binding miR-29b-3p to weaken HMGB1.
{"title":"Suppression of the lncRNA TUG1 alleviates neuropathic pain in rats with chronic contractile injury via the miR-29b-3p/HMGB1 axis.","authors":"Jingjing Dong, Yonghong Ding, Xia Geng, Linkai Jiang, Aiping Ouyang","doi":"10.5114/fn.2024.141512","DOIUrl":"https://doi.org/10.5114/fn.2024.141512","url":null,"abstract":"<p><strong>Introduction: </strong>The present research focused on the function of lncRNA taurine upregulated 1 (TUG1) in a rat neuropathic pain (NP) model constructed by chronic contractile injury (CCI).</p><p><strong>Material and methods: </strong>Construction of the NP rat model was performed by CCI surgery. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were applied to examine the NP behavior. RT-qPCR was established to explore the levels of TUG1, microRNA (miR)-29b-3p, and HMGB1. ELISA was carried out to evaluate the concentrations of interleukin (IL)-6, IL-1β, tumor necrosis factor α (TNF-α), IL-4, and IL-6. The underlying mechanisms of TUG1 were explored by RNA-binding protein immunoprecipitation (RIP) and dual-luciferase reporter (DLR) assay.</p><p><strong>Results: </strong>TUG1 and HMGB1 were statistically elevated in the tissue of CCI rats, while miR-29b-3p was reduced. TUG1 competitively binds to miR-29b-3p to upregulate HMGB1 levels. Suppression of TUG1 persistently decreased PWL and PWT along with increased frequency of paw-lifting, whereas this alleviation was typically rescued by the abrogated miR-29b-3p. Analogously, knockdown of TUG1 inhibited CCI-induced overproduction of IL-6, IL-1β, and TNF-α, and reduction of IL-4 and IL-6, but this inhibition was partially abrogated by the reduction of miR-29b-3p.</p><p><strong>Conclusions: </strong>Suppression TUG1 can alleviate NP hypersensitivity and neuroinflammation in CCI rats by competitively binding miR-29b-3p to weaken HMGB1.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008508","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}
Sevoflurane is an inhalation anaesthetic agent widely used in clinical settings. Despite good surgical outcomes using sevoflurane, patients frequently develop postoperative cognitive dysfunction (POCD). An enriched environment (EE), as a rehabilitation technique, could provide objects and tools to facilitate neuromotor and visual stimuli and brain activity, and is reported to improve cognitive functions. We aim to investigate the impairments of sevoflurane inhalation on cognitive function in mice and determine the benefits of EE in ameliorating POCD. Eighteen-month-old mice were exposed to sevoflurane inhalation for 2 h and then placed in standard environment (SE) or EE cages. The mice without sevoflurane exposure in standard or EE cages were used as controls. The behavioural tests include Morris water maze, Y maze and novel object recognition. Magnetic resonance imaging (MRI) was used to determine the blood circulation in the brains. The proangiogenic factors (CD31, angiopoietin-1, vascular endothelial growth factor, and N-cadherin) and neurotrophic (brain-derived neurotrophic factor, post-synaptic density protein 95) expression in hippocampus of aged mice were evaluated by Western blotting and RT-PCR analysis. Sevoflurane-exposed mice demonstrated reduced performance in learning, memory and spatial memory tests. Enriched environment improved the behavioural performance of sevoflurane-exposed animals. Sevoflurane exposure reduced the blood flow in the brains, and these effects were ameliorated by EE habitation. The EE also promoted the expression of angiogenic and neurotropic factors in sevoflurane-exposed animals. In summary, EE is effective in ameliorating the side-effects of sevoflurane exposure in aged mice.
七氟醚是一种广泛应用于临床的吸入麻醉剂。尽管使用七氟烷能取得良好的手术效果,但患者经常会出现术后认知功能障碍(POCD)。丰富的环境(EE)作为一种康复技术,可提供物品和工具以促进神经运动和视觉刺激以及大脑活动,据报道可改善认知功能。我们旨在研究吸入七氟醚对小鼠认知功能的损害,并确定 EE 对改善 POCD 的益处。将 18 个月大的小鼠吸入七氟醚 2 小时,然后放入标准环境(SE)或 EE 笼中。在标准笼或EE笼中未接触七氟烷的小鼠作为对照组。行为测试包括莫里斯水迷宫、Y迷宫和新物体识别。磁共振成像(MRI)用于确定大脑的血液循环。通过 Western 印迹和 RT-PCR 分析评估了老年小鼠海马中的促血管生成因子(CD31、血管生成素-1、血管内皮生长因子和 N-cadherin)和神经营养因子(脑源性神经营养因子、突触后密度蛋白 95)的表达情况。暴露于七氟烷的小鼠在学习、记忆和空间记忆测试中表现出了能力下降。丰富的环境改善了暴露于七氟烷的动物的行为表现。暴露于七氟烷的小鼠脑血流量减少,而这些影响在居住在 EE 环境中得到了改善。EE 还能促进七氟醚暴露动物体内血管生成因子和神经促进因子的表达。总之,EE 能有效改善七氟醚暴露对老年小鼠的副作用。
{"title":"An enriched environment promotes cognitive recovery and cerebral blood flow in aged mice under sevoflurane anaesthesia.","authors":"Wenfeng Gao, Wenji Xie, Wenqin Xie, Changcheng Jiang, Zhenming Kang, Naizhen Liu","doi":"10.5114/fn.2024.136017","DOIUrl":"https://doi.org/10.5114/fn.2024.136017","url":null,"abstract":"<p><p>Sevoflurane is an inhalation anaesthetic agent widely used in clinical settings. Despite good surgical outcomes using sevoflurane, patients frequently develop postoperative cognitive dysfunction (POCD). An enriched environment (EE), as a rehabilitation technique, could provide objects and tools to facilitate neuromotor and visual stimuli and brain activity, and is reported to improve cognitive functions. We aim to investigate the impairments of sevoflurane inhalation on cognitive function in mice and determine the benefits of EE in ameliorating POCD. Eighteen-month-old mice were exposed to sevoflurane inhalation for 2 h and then placed in standard environment (SE) or EE cages. The mice without sevoflurane exposure in standard or EE cages were used as controls. The behavioural tests include Morris water maze, Y maze and novel object recognition. Magnetic resonance imaging (MRI) was used to determine the blood circulation in the brains. The proangiogenic factors (CD31, angiopoietin-1, vascular endothelial growth factor, and N-cadherin) and neurotrophic (brain-derived neurotrophic factor, post-synaptic density protein 95) expression in hippocampus of aged mice were evaluated by Western blotting and RT-PCR analysis. Sevoflurane-exposed mice demonstrated reduced performance in learning, memory and spatial memory tests. Enriched environment improved the behavioural performance of sevoflurane-exposed animals. Sevoflurane exposure reduced the blood flow in the brains, and these effects were ameliorated by EE habitation. The EE also promoted the expression of angiogenic and neurotropic factors in sevoflurane-exposed animals. In summary, EE is effective in ameliorating the side-effects of sevoflurane exposure in aged mice.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008572","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}
Activation of the NogoA/NgR/ROCK pathway limits nerve repair after brain ischemia-reperfusion (I/R) injury. Triptolide displays anti-inflammatory, anti-oxidant, and immunosuppressive effects and is derived from the traditional Chinese medicine Tripterygium wilfordii Hook F. This agent can also penetrate the blood-brain barrier, where it has a neuroprotective effect and ameliorates cerebral I/R injury via an as yet unknown mechanism(s). Here, an animal model of middle cerebral artery occlusion and reperfusion (MCAO/R) was employed to assess triptolide's therapeutic impact on brain I/R injury and the possible mechanism of action. The results indicate that triptolide treatment can decrease cerebral infarction and nerve injury after cerebral I/R injury. Importantly, in vivo and in vitro experiments revealed that treatment with triptolide decreased NogoA, NgR, p75NTR and ROCK2 expression, and upregulated the expression of GAP43 and PSD-95, thus suggesting improved synaptic function. These results indicate that triptolide can promote nerve repair following brain I/R injury by inhibiting NogoA/NgR/ROCK signalling.
{"title":"Triptolide promotes nerve repair after cerebral ischemia reperfusion injury by regulating the NogoA/NgR/ROCK pathway.","authors":"Huiyu Zhang, Minfang Guo, Peijun Zhang, Bingtao Mu, Zhenjun Bai, Liang Li, Jingwen Yu","doi":"10.5114/fn.2023.133065","DOIUrl":"10.5114/fn.2023.133065","url":null,"abstract":"<p><p>Activation of the NogoA/NgR/ROCK pathway limits nerve repair after brain ischemia-reperfusion (I/R) injury. Triptolide displays anti-inflammatory, anti-oxidant, and immunosuppressive effects and is derived from the traditional Chinese medicine Tripterygium wilfordii Hook F. This agent can also penetrate the blood-brain barrier, where it has a neuroprotective effect and ameliorates cerebral I/R injury via an as yet unknown mechanism(s). Here, an animal model of middle cerebral artery occlusion and reperfusion (MCAO/R) was employed to assess triptolide's therapeutic impact on brain I/R injury and the possible mechanism of action. The results indicate that triptolide treatment can decrease cerebral infarction and nerve injury after cerebral I/R injury. Importantly, in vivo and in vitro experiments revealed that treatment with triptolide decreased NogoA, NgR, p75NTR and ROCK2 expression, and upregulated the expression of GAP43 and PSD-95, thus suggesting improved synaptic function. These results indicate that triptolide can promote nerve repair following brain I/R injury by inhibiting NogoA/NgR/ROCK signalling.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139086560","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}
Piotr Glinka, Michał Sobstyl, Albert Acewicz, Piotr Bojarski
Clear cell meningioma (CCM) is a rare subtype of meningioma, especially unusual as a neoplasm of the filum terminale. Clear cell meningioma seems to have a more aggressive nature and a higher risk of recurrence than WHO grade I meningiomas. A 44-year-old woman presented with lower back pain radiating to the left leg and mild weakness in the left leg. Magnetic resonance imaging (MRI) showed a well-demarcated, intradural lesion filling the spinal canal at the L3-S1 levels and compressing the cauda equina. The patient underwent laminectomy from L3 to S1. During the operation, the filum terminale was identified as a structure that was disappearing into the tumor. The filum terminale was cut and the tumor was totally removed in one piece. Pathological findings were indicative of the diagnosis of clear cell meningioma, CNS WHO G2. Postoperative magnetic resonance imaging at 6 months showed no residual mass. Total surgical excision of the CCM of the spinal cord should be chosen as the optimal treatment. In addition, radiological follow-up is equally important due to the high risk of recurrence. Our case is unusual in that the tumor's location was the filum terminale.
透明细胞脑膜瘤(CCM)是脑膜瘤的一种罕见亚型,作为终丝肿瘤尤为罕见。与世卫组织 I 级脑膜瘤相比,透明细胞脑膜瘤似乎更具侵袭性,复发风险也更高。一名 44 岁的妇女因下腰痛放射至左腿和左腿轻度无力而就诊。磁共振成像(MRI)显示,一个界限清晰的硬膜内病变充满了L3-S1水平的椎管,并压迫马尾。患者接受了从 L3 到 S1 的椎板切除术。在手术过程中,发现终丝结构正在消失在肿瘤中。手术中,患者被发现有一根丝状物消失在肿瘤中,于是切除了丝状物,肿瘤被完整地切除。病理结果显示诊断为透明细胞脑膜瘤,中枢神经系统 WHO G2。术后 6 个月的磁共振成像显示无残留肿块。脊髓透明细胞脑膜瘤的最佳治疗方法是手术全切。此外,由于复发风险高,放射学随访也同样重要。我们的病例与众不同,因为肿瘤位于终丝。
{"title":"Clear cell meningioma of the filum terminale in a 44-year-old woman - case report.","authors":"Piotr Glinka, Michał Sobstyl, Albert Acewicz, Piotr Bojarski","doi":"10.5114/fn.2024.136476","DOIUrl":"https://doi.org/10.5114/fn.2024.136476","url":null,"abstract":"<p><p>Clear cell meningioma (CCM) is a rare subtype of meningioma, especially unusual as a neoplasm of the filum terminale. Clear cell meningioma seems to have a more aggressive nature and a higher risk of recurrence than WHO grade I meningiomas. A 44-year-old woman presented with lower back pain radiating to the left leg and mild weakness in the left leg. Magnetic resonance imaging (MRI) showed a well-demarcated, intradural lesion filling the spinal canal at the L3-S1 levels and compressing the cauda equina. The patient underwent laminectomy from L3 to S1. During the operation, the filum terminale was identified as a structure that was disappearing into the tumor. The filum terminale was cut and the tumor was totally removed in one piece. Pathological findings were indicative of the diagnosis of clear cell meningioma, CNS WHO G2. Postoperative magnetic resonance imaging at 6 months showed no residual mass. Total surgical excision of the CCM of the spinal cord should be chosen as the optimal treatment. In addition, radiological follow-up is equally important due to the high risk of recurrence. Our case is unusual in that the tumor's location was the filum terminale.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008573","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}
Introduction: The morbidity and mortality of spinal cord injury (SCI) are increasing year by year. It is of vital importance to ascertain the mechanism of SCI. Phosphoglycerate mutase family member 5 (PGAM5) is viewed as a molecular marker of SCI, but its specific role in SCI is elusive.
Material and methods: Following establishment of the SCI mouse model, the pathological examination of the spinal cord was initially assessed using H&E staining. PGAM5 expression in spinal cord tissues was appraised utilizing immunohistochemistry and RT-qPCR. Subsequently, after the expression of PGAM5 in SCI mice was inhibited by adenovirus transfection, the degree of SCI was determined, and the motor ability of hind limbs was estimated with the BBB score. In addition, the apoptosis of neurons, microglia activation and the generation of inflammatory cytokines in the spinal cord of mice were detected. Next, at the cellular level, PGAM5 expression was inhibited in the BV2 microglial cells induced by lipopolysaccharide (LPS), so as to explore the effects of down-regulation of PGAM5 on the activation, inflammation and apoptosis of neurons. Finally, western blot was applied for the appraisement of apoptosis signal-regulating kinase-1 (ASK-1)/p38/nuclear factor-kappa B (NF-kB) signaling-associated proteins.
Results: PGAM5 expression in SCI mice was found to be raised. Inhibition of PGAM5 expression in SCI mice can significantly reduce spinal cord pathological injury, SCI-induced neuronal apoptosis, microglial cell activation and inflammation. The above regulatory process might be realized through the ASK-1/p38/NF-kB signaling pathway mediated by PGAM5.
Conclusions: Down-regulation of PGAM5 attenuated SCI-induced neuronal injury by inhibiting ASK-1/p38/NF-kB signaling.
{"title":"Down-regulation of PGAM5 attenuates spinal cord injury-induced neuronal injury by inhibiting ASK-1/p38/NF-kB signaling.","authors":"Junjie Guan, Xin Xu, Runze Zhang, Yingchu Gu, Xiangdong Chen","doi":"10.5114/fn.2024.141372","DOIUrl":"https://doi.org/10.5114/fn.2024.141372","url":null,"abstract":"<p><strong>Introduction: </strong>The morbidity and mortality of spinal cord injury (SCI) are increasing year by year. It is of vital importance to ascertain the mechanism of SCI. Phosphoglycerate mutase family member 5 (PGAM5) is viewed as a molecular marker of SCI, but its specific role in SCI is elusive.</p><p><strong>Material and methods: </strong>Following establishment of the SCI mouse model, the pathological examination of the spinal cord was initially assessed using H&E staining. PGAM5 expression in spinal cord tissues was appraised utilizing immunohistochemistry and RT-qPCR. Subsequently, after the expression of PGAM5 in SCI mice was inhibited by adenovirus transfection, the degree of SCI was determined, and the motor ability of hind limbs was estimated with the BBB score. In addition, the apoptosis of neurons, microglia activation and the generation of inflammatory cytokines in the spinal cord of mice were detected. Next, at the cellular level, PGAM5 expression was inhibited in the BV2 microglial cells induced by lipopolysaccharide (LPS), so as to explore the effects of down-regulation of PGAM5 on the activation, inflammation and apoptosis of neurons. Finally, western blot was applied for the appraisement of apoptosis signal-regulating kinase-1 (ASK-1)/p38/nuclear factor-kappa B (NF-kB) signaling-associated proteins.</p><p><strong>Results: </strong>PGAM5 expression in SCI mice was found to be raised. Inhibition of PGAM5 expression in SCI mice can significantly reduce spinal cord pathological injury, SCI-induced neuronal apoptosis, microglial cell activation and inflammation. The above regulatory process might be realized through the ASK-1/p38/NF-kB signaling pathway mediated by PGAM5.</p><p><strong>Conclusions: </strong>Down-regulation of PGAM5 attenuated SCI-induced neuronal injury by inhibiting ASK-1/p38/NF-kB signaling.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008575","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}
Zihang Xie, Shuxin Zhang, Jie Deng, Shuai Chen, Hua Li, Fangang Meng, Tie Fang
Introduction: This investigation evaluates the effectiveness and safety of stereoelectroencephalography (SEEG)-guided radiofrequency thermocoagulation (RF-TC) as a treatment modality for drug-resistant epilepsy.
Material and methods: A retrospective review of clinical data from 40 paediatric patients with drug-resistant epilepsy, who underwent SEEG-guided RF-TC at our Epilepsy Center between 2020 and 2022, was conducted. This review included the patients' medical history, imaging and electroencephalography results, surgical procedures, and follow-up outcomes.
Results: The duration of SEEG monitoring, accompanied by concurrent electrical stimulation tests, varied from 3 days to 4 weeks. Following RF-TC surgery, 4 patients demonstrated temporary neurological impairments, including central facial and tongue weakness, reduced limb strength, and challenges in fine motor hand movements. All these symptoms were related to lesions in the central region, but showed improvement within 2 weeks to 3 months post-surgery. There were no reported instances of status epilepticus, intracranial haemorrhage, or infections. During a follow-up period of 6 months to 2.5 years, seizure control was achieved in 25 patients (62.5%) at 6 months post-surgery, and a > 50% decrease in seizure frequency was observed in 10 patients. In 5 patients where seizure control was not achieved, the management of epilepsy seemed to be independent of factors such as age at surgery, duration of preoperative disease, seizure type, or negative MRI findings ( p > 0.05). Patients with controlled epilepsy exhibited cognitive improvement, with some demonstrating no EEG abnormalities upon follow-up and a decrease in antiepileptic medication.
Conclusions: SEEG-guided RF-TC appears to be a potentially effective and safe therapeutic approach for paediatric patients with drug-resistant epilepsy.
{"title":"Efficacy and safety of stereoelectroencephalography (SEEG)-guided radiofrequency thermocoagulation (RF-TC) in the treatment of paediatric drug-resistant epilepsy: A retrospective analysis.","authors":"Zihang Xie, Shuxin Zhang, Jie Deng, Shuai Chen, Hua Li, Fangang Meng, Tie Fang","doi":"10.5114/fn.2024.136413","DOIUrl":"https://doi.org/10.5114/fn.2024.136413","url":null,"abstract":"<p><strong>Introduction: </strong>This investigation evaluates the effectiveness and safety of stereoelectroencephalography (SEEG)-guided radiofrequency thermocoagulation (RF-TC) as a treatment modality for drug-resistant epilepsy.</p><p><strong>Material and methods: </strong>A retrospective review of clinical data from 40 paediatric patients with drug-resistant epilepsy, who underwent SEEG-guided RF-TC at our Epilepsy Center between 2020 and 2022, was conducted. This review included the patients' medical history, imaging and electroencephalography results, surgical procedures, and follow-up outcomes.</p><p><strong>Results: </strong>The duration of SEEG monitoring, accompanied by concurrent electrical stimulation tests, varied from 3 days to 4 weeks. Following RF-TC surgery, 4 patients demonstrated temporary neurological impairments, including central facial and tongue weakness, reduced limb strength, and challenges in fine motor hand movements. All these symptoms were related to lesions in the central region, but showed improvement within 2 weeks to 3 months post-surgery. There were no reported instances of status epilepticus, intracranial haemorrhage, or infections. During a follow-up period of 6 months to 2.5 years, seizure control was achieved in 25 patients (62.5%) at 6 months post-surgery, and a > 50% decrease in seizure frequency was observed in 10 patients. In 5 patients where seizure control was not achieved, the management of epilepsy seemed to be independent of factors such as age at surgery, duration of preoperative disease, seizure type, or negative MRI findings ( p > 0.05). Patients with controlled epilepsy exhibited cognitive improvement, with some demonstrating no EEG abnormalities upon follow-up and a decrease in antiepileptic medication.</p><p><strong>Conclusions: </strong>SEEG-guided RF-TC appears to be a potentially effective and safe therapeutic approach for paediatric patients with drug-resistant epilepsy.</p>","PeriodicalId":12370,"journal":{"name":"Folia neuropathologica","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142008576","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}