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Osmotic demyelination syndrome is a pathological condition that leads to electrolyte imbalances and rapid correction, resulting in pseudobulbar palsy, quadriplegia, and altered consciousness. Approximately 33-55％ of affected patients experience residual functional impairment. Herein, we describe a case of a patient with osmotic demyelination syndrome who developed locked-in syndrome during the disease course, underwent rehabilitation treatment, and achieved complete remission without sequelae.The patient was a 47-year-old man who was admitted to hospital A owing to weakness in the lower extremities and dysarthria. He had severe hyponatremia and received sodium correction. However, on hospital day 9, dysarthria redeveloped and involuntary finger movements were noted. Osmotic demyelination syndrome was suspected based on the findings of magnetic resonance imaging of the head and clinical course, leading to his transfer to hospital B. Steroid pulse and rehabilitation therapies were initiated at hospital B. By the 19th day of symptom onset, his limb and facial muscle paralysis progressed, leading to locked-in syndrome. Thereafter, the patient was transferred to hospital C, where he received physiotherapy, occupational therapy, and eating training, markedly improving his physical functions. He was discharged from hospital C, 4 months after the symptom onset, with limited range of motion of the fingers and weakness of the extremities and continued to receive outpatient rehabilitation treatment. His symptoms improved further, and 1 year after the onset of symptoms, he returned to work without any sequelae.
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La esclerosis múltiple (EM) es una enfermedad desmielinizante que afecta el sistema nervioso central. A pesar de los avances en materia de diagnóstico y tratamiento, se desconocen aún muchos aspectos de su etiopatogenia y fisiopatología. La EM es una de las principales causas de discapacidad neurológica y, por los elevados costos de los tratamientos inmunomoduladores e inmunosupresores, tiene un gran impacto económico en la salud pública. Por ello, se intentaron diversos tratamientos preventivos, como la utilización de la vitamina D. Debido a la acción de la vitamina D sobre el sistema inmune, ha sido prescripta en sujetos de riesgo. Sin embargo, hasta el momento actual, los estudios sobre sus efectos no resultaron concluyentes y persisten las dudas acerca de sus posibles beneficios en materia de prevención. El objetivo de la presente revisión bibliográfica es realizar una puesta al día y destacar los aspectos controversiales en relación al uso de la vitamina D como tratamiento preventivo de la esclerosis múltiple. (AU)
Multiple sclerosis (MS) is a demyelinating disease that affects the central nervous system. Despite advances in diagnosis and treatment, many aspects of its etiopathogenesis and pathophysiology remain unknown. MS is one of the main causes of neurological disability and, due to the high costs of modern immunomodulatory and immunosuppressive treatments, it has a great economic impact on public health. Therefore, numerous efforts have been made in the search for preventive treatments. For this reason, various preventive treatments were tried, such as the use of vitamin D. Due to its action on the immune system, it has been used in subjects at ME risk. However, these studies have been inconclusive to date, and its possible benefits in terms of prevention are still being questioned. The objective of this bibliographic review is to update and highlight the controversial aspects in relation to the use of vitamin D as a preventive treatment of multiple sclerosis. (AU)
الموضوعات
Humans , Vitamin D/therapeutic use , Multiple Sclerosis/prevention & control , Vitamin D Deficiency/complications , Immune System/drug effects , Immunity , Multiple Sclerosis/etiologyالملخص
Purpose: Optic neuritis, defined as inflammation of the optic nerve, is the most common optic neuropathy affecting adults. Various studies in Southeast Asia have shown that the clinical profile of optic neuritis might differ in these regions from that reported in the western literature. Through this study, we evaluate the clinical profile of pediatric optic neuritis (PON) in the Indian population. Methods: This was a hospital?based prospective observational study. Patients with optic neuritis younger than 16 years who attended the neuro?ophthalmology clinic from May 2016 to April 2017 were included in the study. Results: This study included 54 eyes of 38 patients. The mean age of presentation was 10.6 years. Unilateral disease (58%) was found to be more common, and a slight female preponderance (58%) was noted. The most common feature was visual loss (96.3%). Pupillary light reflex abnormality was seen in most patients. Fundus examination revealed disk edema (77.7%) to be the most common feature. Neuroimaging was performed in 34 patients, and multiple sclerosis was diagnosed in four patients. At 3 months follow?up after treatment, 89% of eyes had best correct visual acuity of 6/9 or better (P < 0.001). Conclusion: In our study, we found the clinical profile of PON to be similar to that seen in western studies as well as those done previously in the Indian population, although with a few differences
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Resumen Además de provocar problemas respiratorios, la infección con el SARS-CoV-2 puede causar un espectro amplio de complicaciones neurológicas como son cefalea, ageusia, anosmia, encefalopatía, enfermedad cerebrovascular, síndrome de Guillain-Barré y otras polineuropatías, meningoencefalitis, encefalopatía hemorrágica necrotizante aguda y síndromes del sistema nervioso central asociados a inflamación. En esta revisión presentamos 39 casos de mielitis transversa aguda (MTA) asociados a infección por el SARS-CoV-2, confirmado por una prueba de reacción en cadena de la polimerasa (PCR) por hisopado nasofaríngeo y/o de antígeno en plasma. Los análisis bioquímicos de los pacientes confirmaron la ausencia de otros patógenos y de autoanticuerpos involucrados en inflamación del sistema nervioso, excepto por 2 casos, uno con autoanticuerpos contra la glicoproteína de la mielina de los oligodendrocitos (anti-MOG IgG) y otro con anti-MOG IgG y antidescarboxilasa del ácido glutámico (anti-GAD65), indicativos de una enfermedad autoinmune del sistema nervioso central. Los estudios de imagenología de resonancia magnética (RMN) confirmaron el diagnóstico de MTA. Aunque no se puede inferir causalidad, es muy probable que los casos aislados de MTA sean consecuencia de un proceso para o postinfeccioso en la COVID-19. La comprensión de los mecanismos que desencadenan estos trastornos neurológicos durante o al final de la infección viral, ayudarán a optimizar las estrategias terapéuticas para el manejo del paciente.
Abstract In addition to causing respiratory problems, SARS-CoV-2 can cause a wide spectrum of neurological complications such as headaches, ageusia, anosmia, encephalopathy, cerebrovascular disease, Guillain-Barré syndrome and other polyneuropathies, meningoencephalitis, acute necrotizing hemorrhagic encephalopathy, and central nervous system syndromes associated with inflammation. In this review we present 39 cases of acute transverse myelitis (ATM) associated to SARS-CoV-2 infection. All cases had a positive polymerase chain reaction (PCR) nasopharyngeal swab and/or antigen test. Biochemical analyses confirmed the absence of other pathogens and autoantibody-mediated neuroinflammatory disease, except for two cases, one with autoantibodies against the oligodendrocyte myelin glycoprotein (anti-MOG IgG) and another with anti-MOG IgG and anti-glutamic acid decarboxylase (anti-GAD65). Magnetic Resonance Imaging (MRI) studies confirmed the diagnosis of ATM. Although causality cannot be inferred, it is likely that isolated cases of ATM are the consequence of a para or post-infectious process in SARS-CoV-2. In this work, the probable causes of ATM associated with SARS-CoV-2 are discussed. The understanding of the mechanisms behind these neurological disorders triggered by a viral infection will help to optimize the therapeutic strategies for patient management.
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Objective To investigate the imaging and pathological features of intracerebral demyelination pseudotumor(DPT)so as to provide references for clinical diagnosis and treatment.Methods The medical records of 18 intrathecal DPT patients confirmed pathologically in some hospital from May 2010 to March 2021 were analyzed retrospectively,involving in the findings of imaging(MRI and CT),cerebrospinal fluid immunologic examination and histopathologic examination.Results All the patients had the lesions located in the supratentorial brain parenchyma,including 15 ones with single lesions and 3 ones with multiple lesions.In CT images,the lesions had slightly hypodense changes in 13 cases and isodense changes in 5 cases.In MRI images,the lesions showed homogeneous long T1 and long T2 signals in 9 cases,inhomogeneous long T1 and long T2 signals in 7 cases,mixed signals in 2 cases,accompanying cystic degeneration and necrosis in 3 cases,mild edema around the lesions in 10 cases and severe edema in 8 cases;enhanced scans found open ring-like enhancement in 10 cases,nodular enhancement in 6 cases,multiple openings in 2 cases and the long axis of the lesion perpendicular to the lateral ventricle in 8 cases.Immunologic examination of cerebrospinal fluid detected increased content of myelin alkaline protein and positive changes of immunoglobulin G(IgG)at the oligoclonal band.Histopathological examination found a large number of scattered or clustered macrophages in the lesion area and circular lymphocyte infiltration around the blood vessels.Conclusion Intracerebral DPT has the imaging features of open ring-like enhancement and distribution perpendicular to the lateral ventricles and the histopathologic features of macrophage and lymphocyte infiltration.
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Progressive multifocal leukoencephalopathy (PML) is a rare and yet serious central nervous system disorder due to JC viral infection.PML occurs predominantly in immunocompromised individuals, including solid organ transplant (SOT) recipients.Clinically, SOT-related PML commonly presents as cognitive and behavioral impairments. Pathologically, PML is characterized by multifocal demyelinating lesions, with neuroimaging technique typically revealing white matter damage in the temporoparietal regions. Clinical diagnosis usually involves integrating clinical manifestations, cranial magnetic resonance imaging, and detection of JC virus in cerebrospinal fluid. Currently, specific medications for PML are lacking, and the treatment mainly relies on supportive care and immunomodulatory strategies. The prognosis of PML remains unfavorable, early diagnosis and enhanced adaptive immune responses are crucial for PML management in SOT recipients.
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Aim To explore the protective effects of ganoderma lucidum polysaccharides (GLPS) on experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS) and the underlying mechanism. Methods Thirty C57BL/6 mice were randomly divided into three groups: normal control group, EAE model group and GLPS group (5 mg • kg
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Axonal demyelination is an important factor causing neurological dysfunction after spinal cord injury. Retaining the integrity of myelin sheath and promoting remyelination play an important role in the functional recovery of spinal cord injury. The bottleneck of the failure of remyelination is the inability of myelin-forming cells (oligodendrocytes and Schwann cells) to differentiate and mature. In recent years related research on spinal cord injury demyelination has found that cell transplantation, neuregulin-1 and hydrogel can effectively enhance remyelination, and identified aquaporin-4 (aquaporin-4, AQP4), metal-loproteinase (Matrix metailoproteinase, MMP) may be a potential therapeutic target to promote myelin recovery after spinal cord injury. This review discusses the research progress of enhancing remyelination after spinal cord injury, providing ideas for the further development of new methods for the treatment of spinal cord injury.
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OBJECTIVE@#To examine the anti-inflammatory effect of grape seed extract (GSE) in animal and cellular models and explore its mechanism of action.@*METHODS@#This study determined the inhibitory effect of GSE on macrophage inflammation and Th1 and Th17 polarization in vitro. Based on the in vitro results, the effects and mechanisms of GSE on multiple sclerosis (MS)-experimental autoimmune encephalomyelitis (EAE) mice model were further explored. The C57BL/6 mice were intragastrically administered with 50 mg/kg of GSE once a day from the 3rd day to the 27th day after immunization. The activation of microglia, the polarization of Th1 and Th17 and the inflammatory factors such as tumor necrosis factor- α (TNF- α), interleukin-1 β (IL-1 β), IL-6, IL-12, IL-17 and interferon-γ (IFN-γ) secreted by them were detected in vitro and in vivo by flow cytometry, enzyme linked immunosorbent assay (ELISA), immunofluorescence staining and Western blot, respectively.@*RESULTS@#GSE reduced the secretion of TNF-α, IL-1 β and IL-6 in bone marrow-derived macrophages stimulated by lipopolysaccharide (P<0.01), inhibited the secretion of TNF-α, IL-1 β, IL-6, IL-12, IL-17 and IFN-γ in spleen cells of EAE mice immunized for 9 days (P<0.05 or P<0.01), and reduced the differentiation of Th1 and Th17 mediated by CD3 and CD28 factors (P<0.01). GSE significantly improved the clinical symptoms of EAE mice, and inhibited spinal cord demyelination and inflammatory cell infiltration. Peripherally, GSE downregulated the expression of toll-like-receptor 4 (TLR4) and Rho-associated kinase (ROCKII, P<0.05 or P<0.01), and inhibited the secretion of inflammatory factors (P<0.01 or P<0.05). In the central nervous system, GSE inhibited the infiltration of CD45+CD11b+ and CD45+CD4+ cells, and weakened the differentiation of Th1 and Th17 (P<0.05). Moreover, it reduced the secretion of inflammatory factors (P<0.01), and prevented the activation of microglia (P<0.05).@*CONCLUSION@#GSE had a beneficial effect on the pathogenesis and progression of EAE by inhibiting inflammatory response as a potential drug and strategy for the treatment of MS.
الموضوعات
Mice , Animals , Encephalomyelitis, Autoimmune, Experimental/pathology , Grape Seed Extract/therapeutic use , Interleukin-17 , Interleukin-1beta , Tumor Necrosis Factor-alpha/metabolism , Interleukin-6/metabolism , Th1 Cells , Mice, Inbred C57BL , Interferon-gamma/therapeutic use , Th17 Cells/metabolism , Interleukin-12/therapeutic use , Cytokines/metabolismالملخص
Canine Distemper is a disease caused by Canine morbillivirus (CM), a pantropic virus that can affect the central nervous system (CNS), causing demyelination. However, the pathogenesis of this lesion remains to be clarified. Brain samples of 14 naturally infected dogs by CM were analyzed to evaluate the presence of oxidative stress and demyelination. RT-PCR assay was performed to confirm a diagnosis of canine distemper in the brain, immunohistochemistry anti-CM was used to localize the viral proteins in the tissue, and anti-4-hydroxy-2-nonenal (4-HNE) was a marker of a product of lipid peroxidation. The results showed the presence of viral proteins in the demyelinated area with the presence of 4-HNE. Our results suggest that the CM virus infection causes oxidative stress leading to lipid peroxidation, which causes tissue damage and demyelination. In conclusion, oxidative stress plays a significant role in canine distemper pathogenesis in the CNS.(AU)
A cinomose canina é uma doença causada pelo Morbilivírus canino (CM), um vírus pantrópico que pode afetar o sistema nervoso central (SNC), causando desmielinização. No entanto, a patogênese dessa lesão não está totalmente esclarecida. RT-PCR e imuno-histoquímica foram realizadas para confirmação do diagnóstico de cinomose em amostras de encéfalo de 14 cães naturalmente infectados. Após confirmação, foi realizada uma avaliação do estresse oxidativo por imuno-histoquímica com uso de anti-4-hidroxi-nonenal (4HNE) como marcador de produtos resultantes da peroxidação lipídica. Os resultados sugerem que a infecção pelo CM causa estresse oxidativo no tecido, levando a peroxidação lipídica, a qual causa danos ao tecido, culminando com desmielinização. Conclui-se que o estresse oxidativo tem papel importante na patogênese da cinomose canina no sistema nervoso central.(AU)
الموضوعات
Animals , Biomarkers/metabolism , Central Nervous System Infections/veterinary , Distemper/diagnosis , Dogs/virology , Immunohistochemistry/instrumentation , Lipid Peroxidation/drug effects , Demyelinating Diseases/veterinary , Morbillivirus/pathogenicity , Oxidative Stress/physiology , Reverse Transcriptase Polymerase Chain Reaction/instrumentation , Cerebrum/virologyالملخص
Multiple sclerosis ( MS) is an immune-mediated chro¬nic inflammatory disease of the central nervous system (CNS) , which is regulated by multiple pathophysiological mechanisms.There are four clinical phenotypes of MS, including relapsing-re- mitting MS ( RRMS) , primary progressive MS ( PPMS) , sec- ondary-pmgressive MS ( SPMS) , and progressive relapsing MS ( PRMS) , among which RRMS is the main type.'Hie pathogen¬esis of MS is not clear and it could not he cured, so long-term drug treatment is needed for the MS patients.Nowadays, animal models play an important role in the preclinical research of MS drugs.'Hie MS animal models are mainly divided into experi¬mental autoimmune encephalomyelitis (EAE) model, toxin in¬ duced demyelination model, and vims induced demyelination model, among which EAE model is most widely used.'Hie three types of MS animal models demonstrate specific characteristics due to the different induction methods and animal species, and they correspond to specific clinical types of MS.According to the different clinical types of MS, the use of appropriate animal models for drug research and development will help us develop more targeted and potential therapeutic dnrgs, making it possible to cure MS.
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Objective:To explore the effect of low frequency magnetic stimulation on myelin and inflammation in the callosum of demyelinated mice.Methods:Thirty-six 6 to 8-week-old male C57BL/6J mice were randomly divided into a control group, a cuprizone (CPZ) group and a magnetic therapy group. The CPZ group and the magnetic therapy group had demyelination induced by feeding a mixed diet containing 0.3% CPZ for 6 weeks, while the control group was given conventional food. The magnetic therapy group was given 50Hz 10mT magnetic stimulation during the 6 weeks for 20min daily, 5 days a week. The body mass of each mouse was observed every 7 days. At the end of the 6th week elevated cross maze experiments were conducted to observe any anxiety state. The myelin sheath in the corpus callosum was observed using Luxol fast blue staining and myelin basic protein (MBP) immunohistochemistry Tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in the corpus callosum were detected using enzyme-linked immunosorbent assays.Results:After the 6 weeks of treatment, the average body mass of the mice in the magnetic therapy group had improved significantly compared with the CPZ group. The CPZ group′s times in the elevated cross maze experiments were significantly shorter than those of the control group and also shorter than those of the magnetic therapy group. The Luxol staining showed significant myelin loss in the corpus callosum of the CPZ group, but compared with the CPZ group the average loss of myelin in the magnetic therapy group was significantly less. This was further confirmed by the MBP immunohistochemistry. Compared with the control group, the average expression of MBP in the CPZ group was significantly reduced, while in the magnetic therapy group it was significantly increased. Compared with the control group, the average TNF-α and IL-1β levels in the corpus callosum of the CPZ group increased significantly, but compared with the CPZ group the average levels in the magnetic therapy group had decreased significantly.Conclusions:Low frequency magnetic stimulation improves the body weight and anxiety state of mice. That is probably related to less myelin loss and inhibited inflammatory response in the corpus callosum.
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Increasing evidence has shown that astrocytes are implicated in regulating oligodendrocyte myelination, but the underlying mechanisms remain largely unknown. To understand whether microRNAs in astrocytes function in regulating oligodendroglial differentiation and myelination in the developing and adult CNS, we generated inducible astrocyte-specific Dicer conditional knockout mice (hGFAP-CreERT; Dicer fl/fl). By using a reporter mouse line (mT/mG), we confirmed that hGFAP-CreERT drives an efficient and astrocyte-specific recombination in the developing CNS, upon tamoxifen treatment from postnatal day 3 (P3) to P7. The Dicer deletion in astrocytes resulted in inhibited oligodendroglial differentiation and myelination in the developing CNS of Dicer cKO mice at P10 and P14, and did not alter the densities of neurons or axons, indicating that Dicer in astrocytes is required for oligodendrocyte myelination. Consequently, the Dicer deletion in astrocytes at P3 resulted in impaired spatial memory and motor coordination at the age of 9 weeks. To understand whether Dicer in astrocytes is also required for remyelination, we induced Dicer deletion in 3-month-old mice and then injected lysolecithin into the corpus callosum to induce demyelination. The Dicer deletion in astrocytes blocked remyelination in the corpus callosum 14 days after induced demyelination. Together, our results indicate that Dicer in astrocytes is required for oligodendroglia myelination in both the developing and adult CNS.
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The massive loss of oligodendrocytes caused by various pathological factors is a basic feature of many demyelinating diseases of the central nervous system (CNS). Based on a variety of studies, it is now well established that impairment of oligodendrocyte precursor cells (OPCs) to differentiate and remyelinate axons is a vital event in the failed treatment of demyelinating diseases. Recent evidence suggests that Foxg1 is essential for the proliferation of certain precursors and inhibits premature neurogenesis during brain development. To date, very little attention has been paid to the role of Foxg1 in the proliferation and differentiation of OPCs in demyelinating diseases of the CNS. Here, for the first time, we examined the effects of Foxg1 on demyelination and remyelination in the brain using a cuprizone (CPZ)-induced mouse model. In this work, 7-week-old Foxg1 conditional knockout and wild-type (WT) mice were fed a diet containing 0.2% CPZ w/w for 5 weeks, after which CPZ was withdrawn to enable remyelination. Our results demonstrated that, compared with WT mice, Foxg1-knockout mice exhibited not only alleviated demyelination but also accelerated remyelination of the demyelinated corpus callosum. Furthermore, we found that Foxg1 knockout decreased the proliferation of OPCs and accelerated their differentiation into mature oligodendrocytes both in vivo and in vitro. Wnt signaling plays a critical role in development and in a variety of diseases. GSK-3β, a key regulatory kinase in the Wnt pathway, regulates the ability of β-catenin to enter nuclei, where it activates the expression of Wnt target genes. We then used SB216763, a selective inhibitor of GSK-3β activity, to further demonstrate the regulatory mechanism by which Foxg1 affects OPCs in vitro. The results showed that SB216763 clearly inhibited the expression of GSK-3β, which abolished the effect of the proliferation and differentiation of OPCs caused by the knockdown of Foxg1. These results suggest that Foxg1 is involved in the proliferation and differentiation of OPCs through the Wnt signaling pathway. The present experimental results are some of the first to suggest that Foxg1 is a new therapeutic target for the treatment of demyelinating diseases of the CNS.
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@#Objective To investigate the clinical characteristics，imaging manifestations，diagnosis and treatment of patients with bilateral thalamic lesions，so as to improve the understanding of diseases with bilateral thalamic lesions.Methods The clinical datas of 6 patients with bilateral thalamic lesions in our hospital from June 2015 to December 2019 were collected，and the characteristics of each patient were analyzed.Results All 6 patients were with bilateral thalamic lesions，but the diagnosis was different.Case1 was top of the basilar syndrome，case2 was bilateral thalamic infarction（perceron artery occlusion），case3 was deep cerebral venous thrombosis，case 4 was acute disseminated encephalomyelitis，case 5 was Wernicke encephalopathy，and case6 was Wilson’s disease.Conclusion There are many causes of imaging with bilateral thalamic lesions，according to the patient’s clinical characteristics，imaging manifestations，combined with other auxiliary examinations of patients to identify，in order to avoid misdiagnosis.
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Background: Multiple sclerosis (MS) is a neurological disability affecting young and middle-aged adults. Neuropsychiatric manifestations in the background of multiple sclerosis had been reported as a sporadic occurrence. Case description: Here, we report the case of a 57-year-old man who developed neuropsychiatric manifestations during the course of MS. Discussion: In our case, the presence of MS might be a possible reason for the neuropsychiatric manifestations. However, not many case reports have previously acknowledged wherein a patient developed neuropsychiatric symptoms secondary to multiple sclerosis. Conclusion: Hence, this case stresses the need for future studies assessing the relationship between multiple sclerosis and psychosis.
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Multiple sclerosis (MS) is an autoimmune, demyelinating, inflammatory disease of central nervoussystem (CNS) which is characterized by spasticity, fatigue, depression, anxiety, bowel and bladderdysfunction, impaired mobility, cognitive impairment etc. and affects approximately 2.5 million peopleworldwide. Disease modifying therapies for MS which help in preventing accumulation of lesions inwhite matter of CNS are costly and have significant adverse effects. Therefore, patients with MS are usingcomplementary and alternative medicine (CAM) and Yoga is one of the most popular form of CAM whichis being used immensely to reduce or overcome the symptoms of MS. In the current review attempted topresent the potential impact of yoga practices on reducing MS related symptoms.© 2019 The Authors. Published by Elsevier B.V. on behalf of Institute of Transdisciplinary Health Sciencesand Technology and World Ayurveda Foundation. This is an open access article under the CC BY-NC-ND
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Abstract Neurocysticercosis (NCC) is classified as a neglected tropical disease, which affects mainly Latin America and Africa in spite of some reports in North America and Europe. NCC represents the cause of up to 30% of the reported cases of epilepsy in endemic countries. The NCC injuries present direct relation to the development stage, location, and number of parasites as well as to the host immune response. This study aimed the characterization of the inflammatory response and tissue injuries by means of the analyses of the periventricular and parenchymatous demyelination through the experimental intraventricular NCC infection. Therefore, BALB/c mice were submitted to experimental NCC inoculation with Taenia crassiceps cysticerci. Their brains were removed at 7, 30, 60, and 90 days after the inoculation (DAI), and analyzed after staining with hematoxylin and eosin (HE), Luxol Fast Blue, and Nissl. It was possible to observe ventriculomegaly, inflammatory infiltration composed by polymorphonuclear and mononuclear cells, and foamy macrophages. The presence of inflammatory cells was associated with neurodegeneration detected by the areas with demyelination observed initially in the periventricular area and lately in the parenchyma. In conclusion, the presence of cysticerci and the consequent inflammation were able to promote initial periventricular demyelination followed by parenchymatous demyelination as the infection progressed.
Resumo A neurocisticercose (NCC) é classificada como uma doença tropical negligenciada que afeta principalmente a América Latina e a África, apesar de alguns relatos na América do Norte e na Europa. A NCC é responsável por cerca de 30% dos casos de epilepsia em países endêmicos. Estas lesões parecem ter estreita relação com o estádio de desenvolvimento, com a localização e o número de parasitas, bem como a resposta imune do hospedeiro. O presente estudo objetivou caracterizar a resposta de células inflamatórias e as lesões teciduais pela análise da desmielinização periventricular e parenquimatosa ao longo da infecção experimental de NCC intraventricular. Para tanto, camundongos BALB/c foram submetidos a NCC experimental através da inoculação de cisticercos de Taenia crassiceps. O encéfalo foi retirado aos 7, 30, 60 e 90 dias após inoculação (DAI) e analisado após coloração por Hematoxilina e Eosina (HE), Luxol Fast Blue e Nissl. Observou-se ventriculomegalia, processo de infiltração inflamatório composto por células polimorfonucleares, mononucleares e macrófagos espumosos. A presença de células inflamatórias foi associada com neurodegeneração, observada pelas áreas de desmielinização que foram inicialmente periventricular e mais tardiamente no parênquima. Em conclusão, observa-se que a presença dos cisticercos e a inflamação foram capazes de promover desmielinização periventricular inicial e parenquimatosa conforme houve progressão tardia da infecção.
الموضوعات
Animals , Rats , Demyelinating Diseases , Neurocysticercosis , Taenia , Mice, Inbred BALB Cالملخص
Objective: To investigate the repair effect of cannabinoid (WIN55212-2) on the myelin sheath of the demyelination model mice induced by cuprizone, and to elucidate its possible mechanism. Methods: A total of 95 C57BL/6 mice were randomly divided into blank control group, model group (0.2% cuprizone for 6 weeks), DMSO group (intraperitoneally injected with the same amount of DMSO mixture from the 3rd week of feeding 0.2% cuprizone) and treatment group (intraperitoneally injected with 1 mg · kg-1 WIN55212-2 from the 3rd week of feeding 0.2% cuprizone). The myelin sheath tissue of the mice was stained by Black-gold II staining technique, and its histomorphology was observed. The expression levels of juxtanodin (JN), myelin basic protein (MBP) and Nkx2. 2 proteins in mouse brain tissue were detected by Western blotting method. Results: The results of Black-gold I staining showed that the corpus callosum of the brain of the mice in blank control group had significant coloration, while the corpus callosum of the mice in model group showed less coloration. Compared with blank control group, the expression levels of JN and MBP proteins in brain tissue of the mice in model group were significantly decreased (P<0.05). Compared with model group and DMSO group, the expression level of JN and Nkx2. 2 proteins in brain tissue of the mice in treatment group were significantly increased (P