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The correlation between neurodegenerative diseases and the gut microbiome is increasingly evident, with amyotrophic lateral sclerosis (ALS) being particularly notable for its severity and lack of therapeutic options. The gut microbiota, implicated in the pathogenesis and development of ALS, plays a crucial role in the disease. Bioactive plant molecules, specifically volatile compounds in essential oils, offer a promising therapeutic avenue due to their anti-inflammatory properties and gut-modulating effects. Our narrative review aimed to identify microbiota-associated bacteria in ALS and analyze the benefits of administering bioactive plant molecules as much-needed therapeutic options in the management of this disease. A comprehensive search of PubMed database articles published before December 2023, encompassing research on cell, human, and animal ALS models, was conducted. After selecting, analyzing, and discussing key articles, bacteria linked to ALS pathogenesis and physiopathology were identified. Notably, positively highlighted bacteria included Akkermansia muciniphila (Verrucomicrobia phylum), Faecalibacterium prausnitzii, and Butyrivibrio spp. (Firmicutes phylum). Conversely, members of the Escherichia coli spp. (Proteobacteria phylum) and Ruminococcus spp. (Firmicutes phylum) stood out negatively in respect to ALS development. These bacteria were associated with molecular changes linked to ALS pathogenesis and evolution. Bioactive plant molecules can be directly associated with improvements in the microbiome, due to their role in reducing inflammation and oxidative stress, emerging as one of the most promising natural agents for enriching present-day ALS treatments.
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Amyotrophic lateral sclerosis (ALS) is a grievous neurodegenerative disease whose survival is limited to only a few years. In spite of intensive research to discover the underlying mechanisms, the results are fairly inconclusive. Multiple hypotheses have been regarded, including genetic, molecular, and cellular processes. Notably, oxidative stress has been demonstrated to play a crucial role in ALS pathogenesis. In addition to already recognized and exhaustively studied genetic mutations involved in oxidative stress production, exposure to various environmental factors (e.g., electromagnetic fields, solvents, pesticides, heavy metals) has been suggested to enhance oxidative damage. This review aims to describe the main processes influenced by the most frequent genetic mutations and environmental factors concurring in oxidative stress occurrence in ALS and the potential therapeutic molecules capable of diminishing the ALS related pro-oxidative status.
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Esclerose Lateral Amiotrófica , Doenças Neurodegenerativas , Praguicidas , Esclerose Lateral Amiotrófica/etiologia , Campos Eletromagnéticos , Humanos , Doenças Neurodegenerativas/complicações , Estresse OxidativoRESUMO
The neurologic complications of COVID-19 infection are frequent in hospitalized patients; a high percentage of them present neurologic manifestations at some point during the course of their disease. Headache, muscle pain, encephalopathy and dizziness are among the most common complications. Encephalitis is an inflammatory condition with many etiologies. There are several forms of encephalitis associated with antibodies against intracellular neuronal proteins, cell surfaces or synaptic proteins, referred to as autoimmune encephalitis. Several case reports published in the literature document autoimmune encephalitis cases triggered by COVID-19 infection. Our paper first presents our experience in this issue and then systematically reviews the literature on autoimmune encephalitis that developed in the background of SARS-CoV-2 infections and also discusses the possible pathophysiological mechanisms of auto-immune-mediated damage to the nervous system. This review contributes to improve the management and prognosis of COVID-19-related autoimmune encephalitis.
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Stroke is the primary cause of disability in the adult population. Hypertension represents the leading risk factor being present in almost half the patients. The renin-angiotensin system is involved in the physiopathology of stroke and has an essential impact on hypertension as a risk factor. This article targeted the role of the renin-angiotensin system in stroke neuroprotection by reviewing the current literature available. The mechanism of action of the renin-angiotensin system was observed through the effects on AT1, AT2, and Mas receptors. The neuroprotective properties ascertained by angiotensin in stroke seem to be independent of the blood pressure reduction mechanism, and include neuroregeneration, angiogenesis, and increased neuronal resistance to hypoxia. The future relationship of stroke and the renin-angiotensin system is full of possibilities, as new agonist molecules emerge as potential candidates to restrict the impairment caused by stroke.
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Hipertensão , Acidente Vascular Cerebral , Humanos , Hipertensão/tratamento farmacológico , Neuroproteção , Sistema Renina-Angiotensina/fisiologia , Acidente Vascular Cerebral/tratamento farmacológico , Acidente Vascular Cerebral/prevenção & controleRESUMO
The mainstay of cerebral venous thrombosis (CVT) treatment according to current guidelines is parenteral anticoagulation with unfractionated heparin or low-molecular-weight heparin followed by long-term oral anticoagulation with vitamin K antagonists. Direct oral anticoagulants (DOACs), including the factor Xa inhibitor rivaroxaban, are used occasionally off-label for CVT based on individual treatment plans. This publication sought to report our experience with rivaroxaban for the indication of CVT and to review the relevant literature data concerning this topic. We performed a single-center retrospective analysis including patients from our institution with the diagnosis of cerebral venous thrombosis treated with rivaroxaban. Among 12,500 stroke patients over an 11-year period, we identified 87 cases with a diagnosis of CVT (0.7%). As long-term anticoagulation, 80 of these patients were receiving vitamin K antagonists and seven were receiving DOACs, including six receiving rivaroxaban and one receiving apixaban. Of the six patients receiving rivaroxaban, at least 6 months of clinical follow-up data were available for five of them. Excellent clinical outcomes were obtained in four of these five cases (modified Rankin scale score: 0-1 points). No hemorrhagic events, recurrent thrombosis, or other relevant complications were recorded during the follow-up period. Despite our small study sample size, our positive results support that rivaroxaban may be a safe and effective treatment option for patients with CVT. Hopefully, ongoing randomized clinical trials will better clarify the role of rivaroxaban in the treatment of CVT so as to provide a more convenient and safer alternative to vitamin K antagonists in this context.
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Inibidores do Fator Xa/uso terapêutico , Trombose Intracraniana/tratamento farmacológico , Rivaroxabana/uso terapêutico , Idoso , Anticoagulantes/uso terapêutico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Resultado do Tratamento , Trombose Venosa/tratamento farmacológico , Adulto JovemRESUMO
Acute Motor Axonal Neuropathy (AMAN) is an immune-mediated disorder of the peripheral nervous system, part of the spectrum of the Guillain-Barre syndrome (GBS). An infectious event most often triggers it reported a few weeks before the onset. The reported case is of a 56 years-old woman who developed acute motor axonal neuropathy three weeks after respiratory infection with influenza A virus subtype H1N1. Despite early treatment with plasmapheresis and intravenous immunoglobulins, the patient remained tetraplegic, mechanically ventilated for five months, with repetitive unsuccessful weaning trails. The probable cause was considered to be phrenic nerve palsy in the context of acute motor axonal neuropathy. This case highlights that acute motor axonal neuropathy is a severe and life-threatening form of Guillain-Barre syndrome associated with significant mortality and morbidity. Neurological and physical recovery strongly depend on the inter-professional effort in an intensive care unit and neurology professionals.
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OBJECTIVES: To investigate the relationship between neurophysiological sensory and motor nerve function parameters, assessed by nerve conduction studies (NCS) with parasympathetic autonomic function and by heart rate variability (HRV) tests in patients with type 2 diabetes mellitus (T2DM). MATERIAL AND METHODS: A total of 161 T2DM patients underwent NCS. Cardiac autonomic response was assessed by HRV tests to deep breathing (HRV DB), to Valsalva manoeuvre, and during postural change from lying to standing. RESULTS: The amplitude of motor response in the median nerve, tibial nerve, and peroneal nerve was associated with reduced HRV DB (p = 0.0001). The amplitude of motor response in the median nerve, tibial nerve, and peroneal nerve was associated with reduced HRV Valsalva (p = 0.0001). The correlation between the amplitude of response in all sensory nerves (sural, median, and ulnar) and HRV DB was statistically significant (p = 0.0001). CONCLUSION: The results indicate that there is a correlation in T2DM patients between the damage of small myelinated and unmyelinated nerve fibres from cardiac autonomic nerves, assessed by HRV tests and damage of large motor and sensory fibres, assessed by NCS. Based on the above results, a combination of NCS and HRV tests should be considered in the neurophysiological approach to diabetic neuropathy.
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INTRODUCTION: An increasing trend of cancer associated stroke has been noticed in the past decade. OBJECTIVES: To evaluate the risk factors and the incidence of neoplasia in stroke patients. MATERIAL AND METHOD: A retrospective, observational study was undertaken on 249 patients with stroke and active cancer (SAC) and 1563 patients with stroke without cancer (SWC). The general cardiovascular risk factors, the site of cancer, and the general clinical data were registered and evaluated. According to the "Oxfordshire Community Stroke Project" (OCSP) classification, all patients were classified into the clinical subtypes of stroke. The aetiology of stroke was considered as large-artery atherosclerosis, small vessel disease, cardio-embolic, cryptogenic or other determined cause. RESULTS: The severity of neurological deficits at admission were significantly higher in the SAC group (p<0.01). The haemoglobin level was significantly lower, and platelet level and erythrocyte sedimentation rate were significantly higher in the SAC group. Glycaemia, cholesterol and triglycerides levels were significantly higher in the SWC group. The personal history of hypertension was more frequent in the SWC group. In the SAC group, 28.9% had a cryptogenic aetiology, compared to 9.1% in SWC group. Cardio-embolic strokes were more frequent in the SAC group (24%) than the SWC group (19.6%). In the SAC group, 15,6% were diagnosed with cancer during the stroke hospitalization, and 78% of the SAC patients were without metastasis. CONCLUSIONS: The most frequent aetiologies of stroke in cancer patients were cryptogenic stroke, followed by large-artery atherosclerosis. SAC patients had more severe neurological deficits and worse clinical outcomes than SWC patients. Stroke in cancer patients appears to be more frequently cryptogenic, probably due to cancer associated thrombosis. The association between stroke and cancer is important, especially in stroke of cryptogenic mechanism, even in the presence of traditional cardiovascular risk factors.
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INTRODUCTION: Contrast-induced encephalopathy represents a rare, reversible complication that appears after intravenous or intra-arterial exposure to contrast agents. There is no consensus in the literature regarding the mechanism of action. However, the theoretical mechanism is set around the disruption of the blood-brain barrier and the contrast agents' chemical properties. CASE REPORT: The case of a 70-year-old patient, known to have hypertension and type 2 diabetes mellitus is reported. The patient had undergone a diagnostic coronary angiography during which he received 100ml of Ioversol (Optiray 350™). Soon after the procedure, the patient began experiencing a throbbing headache, followed by intense behavioural changes and aggressive tendencies. He was transferred to the Neurology Clinic. The neurological examination was without focal neurological signs; however, the patient was very aggressive and uncooperative. The CT scan revealed a mild hyper-density in the frontal lobes. MRI scan revealed no pathological changes. Conservative treatment with diuretics and hydration was administered, and the patient experienced a complete resolution of symptoms in 72 hours. CONCLUSION: Contrast-induced encephalopathy is a possible secondary complication to contrast agents and a diagnostic challenge, and it should not be overlooked, especially following procedures that use contrast agents.
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There are no published clinical studies regarding the prevalence of subclavian steal among acute ischemic stroke patients. The aim of this study was to evaluate the prevalence and clinical significance of subclavian steal among a large number of consecutive ischemic stroke patients. MATERIALS AND METHODS: We reviewed the medical records of 2192 consecutive cases of acute ischemic stroke at a tertiary neurology clinic in Targu Mures, Romania, between 2018 and 2020. In total, 47 patients (2.2%) were diagnosed with subclavian steal phenomenon/syndrome. RESULTS: Stroke patients with associated steal phenomenon were significantly younger (64.2 ± 11.1 versus 70.2 ± 12.8, p = 0.005) and predominantly male (68.1%). From among the 47 patients with subclavian steal phenomenon, nine (19.1%) presented stroke symptomatology in the vertebrobasilar territory. Overall, 83.3% of the stroke patients with associated steal phenomenon presented cerebral infarction and 16.7% presented TIA. There was no difference between groups regarding the affected vascular territory (VB versus carotid). Large artery atherosclerosis was more frequent in the stroke group with associated steal phenomenon (81.3% versus 43.5%, p = 0.0033). The NIHSS score at admission was higher in the patient group with associated steal phenomenon, but there was no difference in mRS at discharge. Associated carotid artery occlusion was more frequent in the stroke group with steal phenomenon (p < 0.01). Smoking and peripheral arteriopathy were more frequent in the patient group with associated steal phenomenon. Of the nine symptomatic patients, five underwent revascularization treatment. CONCLUSIONS: The prevalence of subclavian steal phenomenon among acute ischemic stroke patients was not higher than in other cohorts with heterogenous peripheral vascular pathologies. Similar to the general population, in acute ischemic stroke patients, the associated subclavian steal behaved like a benign hemodynamical condition, without severe consequences.
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Stroke represents the primary debilitating disease in adults and is the second-highest cause of death worldwide. Atherosclerosis, the most prevalent etiology for vascular conditions, is a continuous process that gradually creates and develops endothelial lesions known as atherosclerotic plaques. These lesions lead to the appearance of atherothrombotic stroke. In the last decades, the role of biological biomarkers has emerged as either diagnostic, prognostic, or therapeutic targets. This article aims to create a list of potential biomarkers related to atherothrombotic stroke by reviewing the currently available literature. We identified 23 biomarkers and assessed their roles as risk factors, detection markers, prognostic predictors, and therapeutic targets. The central aspect of these biomarkers is related to risk stratification, especially for patients who have not yet suffered a stroke. Other valuable data are focused on the predictive capabilities for stroke patients regarding short-term and long-term prognosis, including their influence over the acute phase treatment, such as rt-PA thrombolysis. Although the role of biomarkers is anticipated to be of extreme value in the future, they cannot yet compete with traditional stroke neuroimaging markers but could be used as additional tools for etiological diagnosis.
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Aterosclerose/complicações , Biomarcadores/sangue , Acidente Vascular Cerebral/sangue , Acidente Vascular Cerebral/etiologia , Trombose/complicações , Animais , HumanosRESUMO
Stroke is a leading cause of death and disability worldwide. In addition to the classical etiologies of stroke as atherosclerosis and cardioembolism there are many unusual, rare causes, which require a high level of clinical suspicion and further investigations for correct and early diagnosis and adequate treatment. Giant-cell arteritis or temporal arteritis, the most frequent vasculitis in the elderly population is one of the uncommon causes of stroke. In the setting of giant-cell arteritis, stroke more likely affects the vertebrobasilar territory and is the main cause of mortality. Duplex ultrasound examination is a routine investigation for stroke patients and may be key to the diagnosis if the classical hypoechoic 'halo sign' is recognized at the level of vertebral arteries. In this situation the ultrasound evaluation of temporal arteries and temporal artery biopsy are mandatory. The Giant-cell arteritis-related stroke is a rare condition; therefore, there are no evidence-based guidelines or standard recommendations for the treatment. In the present review, the main characteristics of giant-cell arteritis-related stroke are discussed.
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BACKGROUND: Cerebral venous thrombosis (CVT) is a rare variant of stroke in the general population, but an important subtype among pregnancy- and puerperium-related cases. Studies describing its risk factors and clinical characteristics are limited. The aim of our study is to disclose these aspects and compare with cases unrelated to pregnancy and puerperium. MATERIALS AND METHODS: We performed a retrospective analysis including 88 consecutive cases from a tertiary neurology clinic with a diagnosis of CVT. Ten of the 88 cases (11.3%) appeared during the postpartum period. RESULTS: The mean age of the puerperal CVT cases was 26.5 years. The main pregnancy-related risk factors besides puerperium were cesarean delivery (5/10), preeclampsia (2/10), and stillbirth (1/10). General risk factors for thrombosis, i.e., infection, smoking, and primary hypercoagulability, were identified in 50% of cases. Onset was in the first 3 weeks after delivery, with a mean value of 9.6 ± 5.6 days. Headache was present in 90% of postpartum CVT cases and in 76.1% of non-postpartum female cases. Seizures were more frequent in the postpartum group (60% vs. 34.8%). Onset was acute (<48 h) in 50% of postpartum cases and in 30.4% of the non-postpartum female group. The Rankin score at discharge was significantly lower in the postpartum group (0.22 vs. 0.7, p = 0.02), suggesting a more favorable short-term outcome. CONCLUSIONS: The early postpartum period represents an important risk for the development of CVT. Cesarean delivery and preeclampsia, besides general risk factors such as infection, smoking, and primary thrombophilia, contribute to enhanced risk. Puerperium-related CVT presents a more favorable outcome compared with CVT with other etiologies.
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Gender has been shown to be an important variable in cerebral venous thrombosis (CVT) risk and significantly influences its clinical manifestations and outcome. The aim of our study was to investigate the gender-specific risk factor profile and clinical picture of this rare cerebrovascular disorder. MATERIALS AND METHODS: We retrospectively reviewed the medical records of 89 consecutive cases of CVT at a tertiary neurology clinic in Târgu Mures, Romania, between June 2009 and January 2021 to analyze the gender-related differences in etiology, clinical presentation, and outcome. RESULTS: Women comprised 62.5% of the cohort. Females were significantly younger than males (37.3 years versus 48.8 years, respectively, p = 0.001), and the main risk factors were hormone related in 37.9% of the cases, followed by primary thrombophilia (34.4%), smoking (25.8%), obesity (17.2%), infections (17.2%), mechanical factors (17.2%), cancer (8.6%), systemic autoimmune disorders (8.6%), and hematological disorders (8.6%). In male patients, the main risk factors were smoking (41.9%), primary thrombophilia (29%), infections (22.6%), heavy alcohol consumption (16.1%), and venous thromboembolism in the medical history (12.9%). Frequency of headache was higher in females than in males (75.9% versus 67.7%), whereas frequency of coma (6.5% in males versus 1.7% in females) and dizziness (19.4% in males versus 10.3% in females) was higher in males. CVT onset was acute in 41.4% of females and 38.7% of males. The Rankin score at discharge was significantly lower in females compared with males (0.6 versus 1.6), reflecting a more favorable short-term outcome. Mortality was 6.4% in males and 1.7% in females. CONCLUSIONS: CVT is a multifactorial disorder that has a broad spectrum of risk factors with important gender-related differences in clinical manifestation and prognosis. Female patients, especially those with hormone-related risk factors, have a more favorable outcome than male patients.
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Natalizumab (NAT) was the first disease modifying therapy used for the treatment of relapsing-remitting multiple sclerosis (MS) that was designed with a specific mechanism of action that targets an important step of the MS immunopathology, directly blocking the T lymphocyte intrusion in the central nervous system. Initially, it was considered that NAT carried no biological effects on the peripheral immune response. The purpose of our study was to assess the effects of NAT on the peripheral pro and anti-inflammatory cytokines and to reveal possible correlations between them and the clinical activity of the disease. We noticed a significant decrease in interleukin (IL)-17, tumor necrosis factor-alpha (TNF-α) and IL-31 serum levels in treated patients. The lack of relapses during the study was associated with low baseline IL-17 level. The patients that had an increase in the disability score during the study had significantly lower IL-17 and higher IL-1ß baseline levels. IL-17 can be used as a biomarker for disease activity but also for progression assessment in NAT treated patients. NAT has a far more complex mechanism compared to what was initially believed, besides modulating lymphocyte trafficking through the blood-brain barrier, it also changes the peripheral levels of pro and anti-inflammatory cytokines in MS patients.
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BACKGROUND: Hypokalemic periodic paralysis is a rare skeletal muscle channelopathy characterized by intermittent episodes of acute flaccid paralysis with associated hypokalemia. We present here the case of a first-onset hypokalemic periodic paralysis triggered by lumbar spinal surgery for tumor resection. CASE DESCRIPTION: A 37-year-old male without any known prior medical conditions presented with a first-onset attack of hypokalemic paralysis 1.5 days after lumbar spinal surgery for myxopapillary ependymoma. Initially, the patient presented paraparesis mimicking a spinal cord compression, and while en route for imaging there was an abrupt onset of flaccid paralysis with significant respiratory distress. The emergency blood tests revealed extreme hypokalemia with a serum potassium of 1.42 mm/L. The patient was transferred to the intensive care unit, intubated, sedated, and administered intravenous reperfusion with an infusion dose of 20 mEq/hour potassium in a solution of 5% mannitol. Following reperfusion, the patient recovered completely in 12 hours. Renal potassium hyperexcretion and hyperthyroidism were excluded by laboratory tests. The diagnosis was confirmed by genetic tests showing mutation of the CACNA1S gene. CONCLUSIONS: To the best of our knowledge, this is the first described case with the first onset triggered by a neurosurgical intervention and the second case following any kind of surgery. Neurosurgeons should consider hypokalemic periodic paralysis when encountering a rapidly evolving tetraparesis, even in an apparently healthy patient.
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Ependimoma/cirurgia , Paralisia Periódica Hipopotassêmica/cirurgia , Quadriplegia/cirurgia , Tireotoxicose/cirurgia , Adulto , Ependimoma/complicações , Ependimoma/diagnóstico , Humanos , Paralisia Periódica Hipopotassêmica/diagnóstico , Masculino , Medula Espinal/patologia , Medula Espinal/cirurgia , Tireotoxicose/diagnóstico , Resultado do TratamentoRESUMO
OBJECTIVE: To determine the prevalence of suicidal concerns (SC) in a large multiple sclerosis (MS) patient group and to assess the major determinants that are implicated in their occurrence. METHODS: A total of 349 patients were included in the study. They completed a survey about their demographic characteristics, psycho-socio-economic data, and disease-related information. Their disability level was assessed using the Expanded Disability Status Scale (EDSS) based on the neurological examination performed by the same doctor for every patient and the SC were documented with the Beck Depression Inventory-II questionnaire. RESULTS: The study included 112 men and 237 women, with a mean age around 42 years old. Suicidal thoughts were more frequent in men, while suicidal intentions in women. Positive correlations were found between SC and depression, EDSS, total number of relapses, disease duration, and level of education. From the EDSS functional scores, only the pyramidal score and the cerebellar score presented a significant correlation with SC. None of the patients with clinically isolated syndrome had SC. The type of disease-modifying therapy, marital and occupational status, and the presence of children did not influence the presence of SC. CONCLUSIONS: The prevalence of SC is higher in patients with MS compared to the general population. Their occurrence is mostly influenced by the disease itself (duration, relapses, acquired disability) and also by depression and lack of education.
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Esclerose Múltipla/psicologia , Ideação Suicida , Suicídio/psicologia , Adulto , Estudos de Coortes , Depressão/epidemiologia , Avaliação da Deficiência , Pessoas com Deficiência , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Esclerose Múltipla Recidivante-Remitente/psicologia , Prevalência , Escalas de Graduação Psiquiátrica , Recidiva , Romênia/epidemiologia , Inquéritos e Questionários , Prevenção do SuicídioRESUMO
Th17 cells, known as a highly pro-inflammatory subtype of Th cells, are involved very early in numerous aspects of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) neuropathology. A crucial event for the formation and accumulation of MS lesions is represented by the disruption of the blood brain barrier (BBB) in relapsing-remitting MS. Th17 cells also contribute to the progression of MS/EAE. These events will allow for the passage of inflammatory cells into the brain. Secondary to this, increased recruitment of neutrophils occurs, followed by increased protease activity that will continue to attract macrophages and monocytes, leading to brain inflammation with sustained myelin and axon damage. This review focuses mainly on the role of Th17 cells in penetrating the BBB and on their important effects on BBB disruption via their main secretion products, IL-17 and IL-22. We present the morphological aspects of Th17 cells that allow for intercellular contacts with BBB endothelial cells and the functional/secretory particularities of Th17 cells that allow for intercellular communications that enhance Th17 entry into the CNS. The cytokines and chemokines involved in these processes are described. In conclusion, Th17 cells can efficiently cross the BBB using pathways distinct from those used by Th1 cells, leading to BBB disruption, the activation of other inflammatory cells and neurodegeneration in MS patients.
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Barreira Hematoencefálica/metabolismo , Encefalomielite Autoimune Experimental/imunologia , Encefalomielite Autoimune Experimental/metabolismo , Esclerose Múltipla/imunologia , Esclerose Múltipla/metabolismo , Células Th17/imunologia , Células Th17/metabolismo , Animais , Movimento Celular , Citocinas/metabolismo , Encefalomielite Autoimune Experimental/patologia , Células Endoteliais/metabolismo , Humanos , Esclerose Múltipla/patologia , Células Th1/imunologia , Células Th1/metabolismo , Junções Íntimas/metabolismoRESUMO
INTRODUCTION: There are rare reports of the occurrence of acute transverse myelitis and Guillain-Barré syndrome after various surgical procedures and general/epidural anaesthesia. The concomitant occurrence of these pathologies is very rare and is called Guillain-Barré and acute transverse myelitis overlap syndrome. In this article, we present the case of a second trimester pregnant patient who developed Guillain-Barré and acute transverse myelitis overlap syndrome. CASE PRESENTATION: We report the case of a 16-year-old female patient who underwent a therapeutic termination of pregnancy two weeks prior to the onset of the disease with gradual development of a motor deficit with walking and sensitivity disorders, fecal incontinence. The diagnosis was based on clinical exam, electroneurography and spinal magnetic resonance imaging. Endocrinopathies, infectious diseases, autoimmune and inflammatory diseases, neoplastic diseases and vitamin deficiencies were ruled out. Our patient attended five sessions of therapeutic plasma exchange, followed by steroid treatment, intravenous immunoglobulin with minimum recovery of the motor deficit in the upper limbs, but without significant evolution of the motor deficit in the lower limbs. The patient was discharged on maintenance corticotherapy and immunosuppressive treatment with azathioprine. CONCLUSIONS: We report a very rare association between Guillain-Barré syndrome and acute transverse myelitis triggered by a surgical intervention with general anaesthesia. The overlap of Guillain-Barré syndrome and acute transverse myelitis makes the prognosis for recovery worse, and further studies are needed to establish the first-line therapy in these cases.
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Amyotrophic lateral sclerosis (ALS), an incurable, devastating condition of the central nervous system, is characterized by selective destruction of motoneurons with an important contribution of innate and adaptative immunity. Microglia and immune cells are key players in neuroinflammation and active participants in ALS pathogenesis. Recent experiments in animal models have shown that microglia display both neuroprotective and neurotoxic properties, depending on the stage of disease progression and cytokine secretion. A better knowledge of the interactions between T cells and microglia in the immunopathogenesis of ALS is desirable for the development of ALS therapeutic strategies.