Pub Date : 2021-09-25DOI: 10.31487/j.nnb.2021.03.03
Grace A. Porter, J. O'Connor
Chronic stress is a well-known risk factor in major depressive disorder and disrupts the kynurenine and serotonin pathways of tryptophan metabolism. Here, we characterize the temporal central and peripheral changes in tryptophan metabolism and concomitant depressive-like behavioural phenotype induced during the progression of chronic unpredictable stress (CUS). Mice were exposed to 0, 10, 20, or 30 days of CUS followed by a panel of behavioural assays to determine depressive-like phenotypes. Immediately after behavioural testing, plasma and brain tissue were collected for metabolic analysis. While anhedonia-like and anxiety-like behaviours were unaffected by stress, nesting behaviour and cognitive deficits became apparent in response to CUS exposure. While CUS caused a transient reduction in circulating quinolinic acid, no other tryptophan metabolites significantly changed in response to CUS. In the brain, tryptophan, kynurenine, picolinic acid, and 5-hydroxyindoleacetic acid concentrations were significantly elevated in CUS-exposed mice compared with non-stress control animals, while kynurenic acid, xanthurenic acid, and serotonin decreased in CUS-exposed mice. Metabolic turnover of serotonin to the major metabolite 5- hydroxyindoleacetic acid was markedly increased in response to CUS. These results suggest that CUS impairs hippocampal-dependent working memory and enhances nascent nesting behaviour in C57BL/6J male mice, and these behaviours are associated with increased brain kynurenine pathway metabolism leading to accumulation of picolinic acid and a significant reduction in serotonin levels.
{"title":"Chronic Unpredictable Stress Alters Brain Tryptophan Metabolism and Impairs Working Memory in Mice without Causing Depression-Like Behaviour.","authors":"Grace A. Porter, J. O'Connor","doi":"10.31487/j.nnb.2021.03.03","DOIUrl":"https://doi.org/10.31487/j.nnb.2021.03.03","url":null,"abstract":"Chronic stress is a well-known risk factor in major depressive disorder and disrupts the kynurenine and serotonin pathways of tryptophan metabolism. Here, we characterize the temporal central and peripheral changes in tryptophan metabolism and concomitant depressive-like behavioural phenotype induced during the progression of chronic unpredictable stress (CUS). Mice were exposed to 0, 10, 20, or 30 days of CUS followed by a panel of behavioural assays to determine depressive-like phenotypes. Immediately after behavioural testing, plasma and brain tissue were collected for metabolic analysis. While anhedonia-like and anxiety-like behaviours were unaffected by stress, nesting behaviour and cognitive deficits became apparent in response to CUS exposure. While CUS caused a transient reduction in circulating quinolinic acid, no other tryptophan metabolites significantly changed in response to CUS. In the brain, tryptophan, kynurenine, picolinic acid, and 5-hydroxyindoleacetic acid concentrations were significantly elevated in CUS-exposed mice compared with non-stress control animals, while kynurenic acid, xanthurenic acid, and serotonin decreased in CUS-exposed mice. Metabolic turnover of serotonin to the major metabolite 5- hydroxyindoleacetic acid was markedly increased in response to CUS. These results suggest that CUS impairs hippocampal-dependent working memory and enhances nascent nesting behaviour in C57BL/6J male mice, and these behaviours are associated with increased brain kynurenine pathway metabolism leading to accumulation of picolinic acid and a significant reduction in serotonin levels.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81555276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-08-16DOI: 10.31487/j.nnb.2021.03.02
A. Jaiswal, S. Agrawal, S. Jaiswal, K. Das, S. Behari, S. Tewari, Madam Mohan Godbole, P. Misra
Background: Development of different molecular markers has given a new insight in the glioma management. KIAA1549-BRAF gene fusion has a diagnostic and prognostic significance. Aim: The aim of this study was to determine the KIAA1549-BRAF gene fusion in glioma and their correlation with various clinical parameters. Material and Methods: Forty cases of glioma were studied for KIAA1549-BRAF gene fusion by reverse transcription-PCR (RT-PCR). Results: Overall, KIAA1549-BRAF gene fusion was found in 22% (9/40) cases of glioma. Children had higher KIAA1549-BRAF fusion (72%; 8/11) as compared to adults (10%; 3/29) and this difference was statistically significant. Cerebellar location of tumor was significantly associated with KIAA1549-BRAF fusion. KIAA1549-BRAF fusion was highest in pilocytic astrocytoma (89%), and this difference was statistically significant. Statistically significant difference was noted between KIAA1549-BRAF fusion expression and WHO grade I glioma. Conclusion: Overall, KIAA1549-BRAF gene fusion was found in 22% (9/40) cases of glioma. Childhood age, pilocytic astrocytoma histology, cerebellar location and WHO grade I tumor were significantly associated with KIAA1549-BRAF gene fusion.
{"title":"Evaluation of BRAF Gene Status in Gliomas","authors":"A. Jaiswal, S. Agrawal, S. Jaiswal, K. Das, S. Behari, S. Tewari, Madam Mohan Godbole, P. Misra","doi":"10.31487/j.nnb.2021.03.02","DOIUrl":"https://doi.org/10.31487/j.nnb.2021.03.02","url":null,"abstract":"Background: Development of different molecular markers has given a new insight in the glioma \u0000management. KIAA1549-BRAF gene fusion has a diagnostic and prognostic significance. \u0000Aim: The aim of this study was to determine the KIAA1549-BRAF gene fusion in glioma and their \u0000correlation with various clinical parameters.\u0000Material and Methods: Forty cases of glioma were studied for KIAA1549-BRAF gene fusion by reverse \u0000transcription-PCR (RT-PCR).\u0000Results: Overall, KIAA1549-BRAF gene fusion was found in 22% (9/40) cases of glioma. Children had \u0000higher KIAA1549-BRAF fusion (72%; 8/11) as compared to adults (10%; 3/29) and this difference was \u0000statistically significant. Cerebellar location of tumor was significantly associated with KIAA1549-BRAF\u0000fusion. KIAA1549-BRAF fusion was highest in pilocytic astrocytoma (89%), and this difference was \u0000statistically significant. Statistically significant difference was noted between KIAA1549-BRAF fusion \u0000expression and WHO grade I glioma. \u0000Conclusion: Overall, KIAA1549-BRAF gene fusion was found in 22% (9/40) cases of glioma. Childhood \u0000age, pilocytic astrocytoma histology, cerebellar location and WHO grade I tumor were significantly \u0000associated with KIAA1549-BRAF gene fusion.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79226293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-08-09DOI: 10.31487/j.nnb.2021.03.01
Nasser M Alorfi, S. Dolan
Obesity is associated with several co-morbidities including chronic pain. Systemic low-grade chronic inflammation and dysregulation of pro-inflammatory cytokines have been proposed to underlie these phenomena. This study characterized pain and inflammation, and levels of the pro-inflammatory cytokine visfatin, in a rodent model of obesity, and investigated whether treatment with the visfatin inhibitor, FK866, has anti-inflammatory and/or analgesic effects in normal and obese rats. The effects of pre-administration of FK866 (3, 10 mg/kg; i.p.) on carrageenan (3%; i.d. into the left paw)-induced thermal and mechanical hypersensitivity and paw oedema was measured in adult male Wistar rats fed a normal diet (ND) or high fat diet (HFD) for 12 weeks. HFD-fed rats displayed an increased sensitivity to acute mechanical nociceptive stimulation, and potentiated mechanical hyperalgesia and peripheral inflammation to carrageenan. Levels of circulating visfatin were increased in HFD-fed rats. Treatment with FK866, a visfatin inhibitor, was effective in reducing carrageenan-induced hyperalgesia and paw oedema in both ND-fed and HFD-fed rats. These data show that FK866 has anti-inflammatory and analgesic properties. The potentiated response to pain and inflammation, and elevated visfatin levels in HFD-fed rats supports the hypothesis that obesity is a chronic low-grade inflammatory disorder. Reversal of this co-morbidity by blocking visfatin may be a novel therapeutic strategy for managing pain with obesity.
{"title":"Augmented Pain and Inflammation with Obesity: A Role for the Pro-Inflammatory Cytokine Visfatin","authors":"Nasser M Alorfi, S. Dolan","doi":"10.31487/j.nnb.2021.03.01","DOIUrl":"https://doi.org/10.31487/j.nnb.2021.03.01","url":null,"abstract":"Obesity is associated with several co-morbidities including chronic pain. Systemic low-grade chronic inflammation and dysregulation of pro-inflammatory cytokines have been proposed to underlie these phenomena. This study characterized pain and inflammation, and levels of the pro-inflammatory cytokine visfatin, in a rodent model of obesity, and investigated whether treatment with the visfatin inhibitor, FK866, has anti-inflammatory and/or analgesic effects in normal and obese rats. The effects of pre-administration of FK866 (3, 10 mg/kg; i.p.) on carrageenan (3%; i.d. into the left paw)-induced thermal and mechanical hypersensitivity and paw oedema was measured in adult male Wistar rats fed a normal diet (ND) or high fat diet (HFD) for 12 weeks. HFD-fed rats displayed an increased sensitivity to acute mechanical nociceptive stimulation, and potentiated mechanical hyperalgesia and peripheral inflammation to carrageenan. Levels of circulating visfatin were increased in HFD-fed rats. Treatment with FK866, a visfatin inhibitor, was effective in reducing carrageenan-induced hyperalgesia and paw oedema in both ND-fed and HFD-fed rats. These data show that FK866 has anti-inflammatory and analgesic properties. The potentiated response to pain and inflammation, and elevated visfatin levels in HFD-fed rats supports the hypothesis that obesity is a chronic low-grade inflammatory disorder. Reversal of this co-morbidity by blocking visfatin may be a novel therapeutic strategy for managing pain with obesity.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75169417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-07-30DOI: 10.31487/j.nnb.2021.02.04
N. Mekhail, Youssef Saweris, Lou-Anne Acevedo-Moreno
Objective: To explore whether saline is a real sham/placebo agent, or it has potential therapeutic effects when used as control treatment in randomized controlled trials for the management of discogenic low back pain. Methods: A comprehensive literature search was conducted investigating the effects of saline as a placebo in the treatment of chronic pain when administered into the intervertebral disc. Following stepwise filtering, selected articles were assessed for their levels of evidence, followed by a discussion of their contribution to the understanding of the role of saline in chronic pain management. Results: Out of 95 articles that described the administration of intradiscal saline solution used as a placebo for chronic pain management, 8 articles met all of the inclusion criteria. Their levels of evidence ranged from 1a to 4 (Oxford Centre CEBM). Intradiscal administration of saline solution was found to have measurable therapeutic benefits. In some studies, the pain relief was similar to that provided by local anaesthetics and steroids. Conclusion: Although the exact mechanism of the analgesic effects of saline is not clear, yet the use of intradiscal saline appears to have some analgesic benefits like local anaesthetics and steroids when used individually. Researchers should practice caution when designing RCTs using intradiscal saline injection as a sham/placebo treatment for the control arm or maybe, when possible, avoid the use of intradiscal saline injection as a sham treatment.
{"title":"Is Saline Injection a True Sham/Placebo Treatment in Randomized Controlled Trials? A Systematic Review","authors":"N. Mekhail, Youssef Saweris, Lou-Anne Acevedo-Moreno","doi":"10.31487/j.nnb.2021.02.04","DOIUrl":"https://doi.org/10.31487/j.nnb.2021.02.04","url":null,"abstract":"Objective: To explore whether saline is a real sham/placebo agent, or it has potential therapeutic effects when used as control treatment in randomized controlled trials for the management of discogenic low back pain.\u0000Methods: A comprehensive literature search was conducted investigating the effects of saline as a placebo in the treatment of chronic pain when administered into the intervertebral disc. Following stepwise filtering, selected articles were assessed for their levels of evidence, followed by a discussion of their contribution to the understanding of the role of saline in chronic pain management.\u0000Results: Out of 95 articles that described the administration of intradiscal saline solution used as a placebo for chronic pain management, 8 articles met all of the inclusion criteria. Their levels of evidence ranged from 1a to 4 (Oxford Centre CEBM). Intradiscal administration of saline solution was found to have measurable therapeutic benefits. In some studies, the pain relief was similar to that provided by local anaesthetics and steroids.\u0000Conclusion: Although the exact mechanism of the analgesic effects of saline is not clear, yet the use of intradiscal saline appears to have some analgesic benefits like local anaesthetics and steroids when used individually. Researchers should practice caution when designing RCTs using intradiscal saline injection as a sham/placebo treatment for the control arm or maybe, when possible, avoid the use of intradiscal saline injection as a sham treatment.\u0000","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"22 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83957147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-06-28DOI: 10.31487/j.nnb.2021.02.03
M. Singer
Children born into and raised in disadvantaged families tend to experience poorer health and more developmental delays, lower achievement, and a greater number of behavioural and emotional problems than children from wealthier homes. There is growing evidence that poverty and social inequality leave their imprint on brain structure as well. The brain exhibits considerable plasticity, one expression of which is shaped by the biology of inequality. A specific consequence is cognitive deficit found among children raised in poverty and subject to social discrimination. This paper argues that several pathways impacted by poverty, including chronic stress, malnutrition, exposure to heightened levels of air pollution, and other toxin exposures, syndemically link social inequality to underlying neural mechanisms and to suboptimal brain development and structure. These deficits need not be permanent and are reversible through urgently needed structural, socio-economic intervention.
{"title":"Brain Syndemics: Cognitive Deficit, Pathways of Interaction, and the Biology of Inequality","authors":"M. Singer","doi":"10.31487/j.nnb.2021.02.03","DOIUrl":"https://doi.org/10.31487/j.nnb.2021.02.03","url":null,"abstract":"Children born into and raised in disadvantaged families tend to experience poorer health and more \u0000developmental delays, lower achievement, and a greater number of behavioural and emotional problems \u0000than children from wealthier homes. There is growing evidence that poverty and social inequality leave their \u0000imprint on brain structure as well. The brain exhibits considerable plasticity, one expression of which is \u0000shaped by the biology of inequality. A specific consequence is cognitive deficit found among children raised \u0000in poverty and subject to social discrimination. This paper argues that several pathways impacted by \u0000poverty, including chronic stress, malnutrition, exposure to heightened levels of air pollution, and other \u0000toxin exposures, syndemically link social inequality to underlying neural mechanisms and to suboptimal \u0000brain development and structure. These deficits need not be permanent and are reversible through urgently \u0000needed structural, socio-economic intervention.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81562721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-28DOI: 10.31487/J.NNB.2021.02.02
M. Mahmood, Tiyyaba Furqan, Muaaz Karim, Sidra Batool
Alzheimer’s is a progressive mental deterioration associated with the degeneration of the cognition activities and memory loss. It is considered to be a multifactorial disease. One of the causes of the Alzheimer’s disease is the low concentration of the neurotransmitter named acetylcholine (ACh) at the synaptic cleft. Thus, inhibitor of Acetylcholinesterase (AChE), an enzyme whose function is to degrade the acetylcholine, is proved to be a promising candidate to treat this disease. Among the inhibitors are the natural alkaloids that also have an inhibitory effect on the AChE. In this study we have focused on the simple derivates of beta carbolime (a group of alkaloids) and studied their interaction with AChE via rigid protein-ligand docking approach.
{"title":"In silico Analysis of Alkaloids for Therapeutic Use in Treatment of Alzheimer's Disease by Targeting Acetylcholinesterase Enzyme","authors":"M. Mahmood, Tiyyaba Furqan, Muaaz Karim, Sidra Batool","doi":"10.31487/J.NNB.2021.02.02","DOIUrl":"https://doi.org/10.31487/J.NNB.2021.02.02","url":null,"abstract":"Alzheimer’s is a progressive mental deterioration associated with the degeneration of the cognition activities and memory loss. It is considered to be a multifactorial disease. One of the causes of the Alzheimer’s disease is the low concentration of the neurotransmitter named acetylcholine (ACh) at the synaptic cleft. Thus, inhibitor of Acetylcholinesterase (AChE), an enzyme whose function is to degrade the acetylcholine, is proved to be a promising candidate to treat this disease. Among the inhibitors are the natural alkaloids that also have an inhibitory effect on the AChE. In this study we have focused on the simple derivates of beta carbolime (a group of alkaloids) and studied their interaction with AChE via rigid protein-ligand docking approach.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89796347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-26DOI: 10.31487/J.NNB.2021.02.01
J. Holt, S. Robertson, S. McCrory
Background: We present two patients with the Lewis-Sumner variant of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), charting the diagnostic challenge posed by their clinical presentation and electrodiagnostic findings. The learning points center on the use of magnetic resonance imaging (MRI) in establishing a definitive diagnosis when clinical and neurophysiology data do not otherwise add up. Cases: The first patient presented with slowly progressive asymmetric distal weakness of the lower limbs with wasting, weakness, areflexia and numbness on examination. The second patient experienced stepwise asymmetric hand/forearm weakness with deformity and areflexia, plus mild distal sensory impairment. Neurophysiological studies for both patients were initially most suggestive of mononeuritis multiplex, with no evidence of demyelination. Conclusion: The possibility of asymmetric or multifocal CIDP, the Lewis-Sumner variant, should not be forgotten in suspected mononeuritis multiplex and the value of MRI in such cases is discussed.
{"title":"CIDP Masquerading as Mononeuritis Multiplex: The Value of MR Neurography","authors":"J. Holt, S. Robertson, S. McCrory","doi":"10.31487/J.NNB.2021.02.01","DOIUrl":"https://doi.org/10.31487/J.NNB.2021.02.01","url":null,"abstract":"Background: We present two patients with the Lewis-Sumner variant of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), charting the diagnostic challenge posed by their clinical presentation and electrodiagnostic findings. The learning points center on the use of magnetic resonance imaging (MRI) in establishing a definitive diagnosis when clinical and neurophysiology data do not otherwise add up.\u0000Cases: The first patient presented with slowly progressive asymmetric distal weakness of the lower limbs with wasting, weakness, areflexia and numbness on examination. The second patient experienced stepwise asymmetric hand/forearm weakness with deformity and areflexia, plus mild distal sensory impairment. Neurophysiological studies for both patients were initially most suggestive of mononeuritis multiplex, with no evidence of demyelination.\u0000Conclusion: The possibility of asymmetric or multifocal CIDP, the Lewis-Sumner variant, should not be forgotten in suspected mononeuritis multiplex and the value of MRI in such cases is discussed.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89633222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The diffuse midline glioma, H3K27M-mutant subtype, occurs mainly in children as a result of mutations in the histone H3 (H3F3A) and HIST1H3B (K27M) genes and is characterized by diffuse tumor growth in central nervous system (CNS) midline structures. Due to its nonspecific clinical manifestations, viral encephalitis is often confused with other central nervous system diseases. In this case, we reported a young male patient who was admitted to the hospital chiefly complaining of “diplopia for more than two months and aggravated walking instability for more than 10 days”. After admission, relevant patient blood and cerebrospinal fluid (CSF) tests were completed, and no obvious abnormalities were found. Chest CT suggested pulmonary infection; magnetic resonance imaging (MRI) and contrast-enhanced CT, PET-CT and other imaging examinations of the head all indicated a high possibility of viral encephalitis. Symptoms of fever were improved in the patient after treatment with antiviral therapy and anti-infection therapy. However, symptoms of neurological function loss, such as double vision and adverse right limb movement, persisted. Finally, stereotactic biopsies of deep brain lesions were carried out and sent to the pathology department, which led to a diagnosis of diffuse midline glioma, H3K27M-mutant subtype (WHO IV). His family chose to perform conservative treatment in another hospital, and the patient died four months later. To conclude, when clinical symptoms of suspected viral encephalitis appear in the course of diffuse midline glioma, it can result in confusion regarding clinical diagnosis and treatment. Clinicians should ensure proper early recognition and identification of the disease.
{"title":"Diffuse Midline Glioma, H3K27M-mutant Subtype, Confused for Viral Encephalitis: A Case Report","authors":"Weidong Yang, Cong Fu, Yiyao Cao, Zhi-juan Chen, Qing Yu","doi":"10.31487/J.NNB.2020.04.03","DOIUrl":"https://doi.org/10.31487/J.NNB.2020.04.03","url":null,"abstract":"The diffuse midline glioma, H3K27M-mutant subtype, occurs mainly in children as a result of mutations in\u0000the histone H3 (H3F3A) and HIST1H3B (K27M) genes and is characterized by diffuse tumor growth in\u0000central nervous system (CNS) midline structures. Due to its nonspecific clinical manifestations, viral\u0000encephalitis is often confused with other central nervous system diseases. In this case, we reported a young\u0000male patient who was admitted to the hospital chiefly complaining of “diplopia for more than two months\u0000and aggravated walking instability for more than 10 days”. After admission, relevant patient blood and\u0000cerebrospinal fluid (CSF) tests were completed, and no obvious abnormalities were found. Chest CT\u0000suggested pulmonary infection; magnetic resonance imaging (MRI) and contrast-enhanced CT, PET-CT\u0000and other imaging examinations of the head all indicated a high possibility of viral encephalitis. Symptoms\u0000of fever were improved in the patient after treatment with antiviral therapy and anti-infection therapy.\u0000However, symptoms of neurological function loss, such as double vision and adverse right limb movement,\u0000persisted. Finally, stereotactic biopsies of deep brain lesions were carried out and sent to the pathology\u0000department, which led to a diagnosis of diffuse midline glioma, H3K27M-mutant subtype (WHO IV). His\u0000family chose to perform conservative treatment in another hospital, and the patient died four months later.\u0000To conclude, when clinical symptoms of suspected viral encephalitis appear in the course of diffuse midline\u0000glioma, it can result in confusion regarding clinical diagnosis and treatment. Clinicians should ensure proper\u0000early recognition and identification of the disease.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"36 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82518199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-12-18DOI: 10.31487/j.nnb.2020.03.07
M. Stachowiak, D. Freedman, N. Nived, B. Decker, S. Narla, S. Shafik, S. Manohar, R. Salvi, E. Stachowiak
Neurological manifestations of blast-induced Post Traumatic Stress Disorder (PTSD) extend long after the initial injury indicating lasting changes in brain function. In this study, we characterized brain injury, changes in neurogenesis and oligodendrogenesis in an adult murine blast model following a short (5 days) and long (21 days) post-blast recovery. Acoustic blasts led to an initial, activation of microglia and astrogliosis and a widespread cortical and subcortical apoptosis. The loss of myelinated cortical axons at 5 days was followed by the reappearance of abnormal misdirected fibers at 21 days. At 21 days post-blast, we observed increases in doublecortin-positive (DCX+ ) neuroblasts in the subventricular zone (SVZ) and hippocampal subgranular zone (SGZ) indicating increased neurogenesis. No changes in DCX+ cells were found in the brain cortex. In the cortex, the early disappearance of myelinated neuronal fibers was accompanied by a loss of O4+ oligodendrocytes and their Ki67-expreasing (Ki67+ ) oligodendrocyte precursor cells (OPC). However, at 5 days we observed a robust appearance of cells expressing Olig2 (O2+ ), an early determinant of oligodendrocyte lineage. At 21 days post-blast, the population of OPC increased and the mature O4+ oligodendrocytes were restored to control levels. In contrast, in the SVZ and SGZ, O4+ cells were not affected by the blast suggesting a local cortical origin for cortical oligodendrogenesis. These results suggest that blast-induced activation of SVZ and SGZ neurogenesis and cortical oligodendrogenesis could have long-lasting impact on brain function including memory disorders observed in both animal models and human’s PTSD.
{"title":"Neurogenesis and Oligodendrogenesis in a Mouse Model of Blast-Induced Traumatic Brain Injury","authors":"M. Stachowiak, D. Freedman, N. Nived, B. Decker, S. Narla, S. Shafik, S. Manohar, R. Salvi, E. Stachowiak","doi":"10.31487/j.nnb.2020.03.07","DOIUrl":"https://doi.org/10.31487/j.nnb.2020.03.07","url":null,"abstract":"Neurological manifestations of blast-induced Post Traumatic Stress Disorder (PTSD) extend long after the\u0000initial injury indicating lasting changes in brain function. In this study, we characterized brain injury,\u0000changes in neurogenesis and oligodendrogenesis in an adult murine blast model following a short (5 days)\u0000and long (21 days) post-blast recovery. Acoustic blasts led to an initial, activation of microglia and\u0000astrogliosis and a widespread cortical and subcortical apoptosis. The loss of myelinated cortical axons at 5\u0000days was followed by the reappearance of abnormal misdirected fibers at 21 days. At 21 days post-blast, we\u0000observed increases in doublecortin-positive (DCX+\u0000) neuroblasts in the subventricular zone (SVZ) and\u0000hippocampal subgranular zone (SGZ) indicating increased neurogenesis. No changes in DCX+\u0000cells were\u0000found in the brain cortex. In the cortex, the early disappearance of myelinated neuronal fibers was\u0000accompanied by a loss of O4+ oligodendrocytes and their Ki67-expreasing (Ki67+\u0000) oligodendrocyte\u0000precursor cells (OPC). However, at 5 days we observed a robust appearance of cells expressing Olig2 (O2+\u0000),\u0000an early determinant of oligodendrocyte lineage. At 21 days post-blast, the population of OPC increased\u0000and the mature O4+ oligodendrocytes were restored to control levels. In contrast, in the SVZ and SGZ, O4+\u0000cells were not affected by the blast suggesting a local cortical origin for cortical oligodendrogenesis. These\u0000results suggest that blast-induced activation of SVZ and SGZ neurogenesis and cortical oligodendrogenesis\u0000could have long-lasting impact on brain function including memory disorders observed in both animal\u0000models and human’s PTSD.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"8 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80040288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-24DOI: 10.31487/j.nnb.2020.03.09
N. Mekhail, Shrif J Costandi, A. Abd-Elsayed, G. Fiore, Jijun Xu, Lou-Anne Acevedo-Moreno, L. Kapural, A. Rezai, C. Gilligan
Objective: Exploring the potential role of clonidine as an alternative to the currently available neuraxial medication options for the management of chronic pain. Methods: A comprehensive literature search was conducted investigating the treatment of chronic pain using clonidine over the past 73 years. A stepwise filtering approach was used to obtain articles addressing neuraxial treatment of chronic pain in adults. Selected articles were assessed for their levels of evidence followed by a discussion of their contribution to the understanding of the role of clonidine in chronic pain management. Results: Out of 1,035 articles that described the administration of clonidine for chronic pain management, seven articles met all of the inclusion criteria. Their levels of evidence ranged from 1a to 4 (Oxford Centre CEBM). Neuraxial administration of clonidine was found to be effective in the treatment of chronic pain, often exhibiting a synergistic effect with other analgesics to provide pain reduction with reduced opioid use. The most common side effect was hypotension, in some cases reported to have been serious. Conclusion: The use of neuraxial clonidine, in either a primary or adjunctive role, appears promising as an effective treatment for chronic pain.
{"title":"Is Neuraxial Clonidine a Safer Alternative to Opioids for Chronic Pain? An Alternative Worth Exploring","authors":"N. Mekhail, Shrif J Costandi, A. Abd-Elsayed, G. Fiore, Jijun Xu, Lou-Anne Acevedo-Moreno, L. Kapural, A. Rezai, C. Gilligan","doi":"10.31487/j.nnb.2020.03.09","DOIUrl":"https://doi.org/10.31487/j.nnb.2020.03.09","url":null,"abstract":"Objective: Exploring the potential role of clonidine as an alternative to the currently available neuraxial\u0000medication options for the management of chronic pain.\u0000Methods: A comprehensive literature search was conducted investigating the treatment of chronic pain\u0000using clonidine over the past 73 years. A stepwise filtering approach was used to obtain articles addressing\u0000neuraxial treatment of chronic pain in adults. Selected articles were assessed for their levels of evidence\u0000followed by a discussion of their contribution to the understanding of the role of clonidine in chronic pain\u0000management.\u0000Results: Out of 1,035 articles that described the administration of clonidine for chronic pain management,\u0000seven articles met all of the inclusion criteria. Their levels of evidence ranged from 1a to 4 (Oxford Centre\u0000CEBM). Neuraxial administration of clonidine was found to be effective in the treatment of chronic pain,\u0000often exhibiting a synergistic effect with other analgesics to provide pain reduction with reduced opioid use.\u0000The most common side effect was hypotension, in some cases reported to have been serious.\u0000Conclusion: The use of neuraxial clonidine, in either a primary or adjunctive role, appears promising as an\u0000effective treatment for chronic pain.","PeriodicalId":19179,"journal":{"name":"Neurology and Neurobiology","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90270052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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