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1.
Rev Med Suisse ; 16(692): 904-906, 2020 May 06.
Artigo em Francês | MEDLINE | ID: mdl-32374534

RESUMO

Spasticity is a common sign of central nervous system lesions and its management is difficult because it is usually associated with other symptoms of upper motoneuron syndrome (paresis, spastic dystonia, contractures, …). We propose an interprofessional evaluation, which demonstrates that a standardized evaluation, a common approach and a gait analysis improve the therapeutic decision.


Assuntos
Sistema Nervoso Central/lesões , Sistema Nervoso Central/fisiopatologia , Espasticidade Muscular/diagnóstico , Espasticidade Muscular/terapia , Análise da Marcha , Humanos , Espasticidade Muscular/fisiopatologia
2.
ACS Chem Neurosci ; 11(7): 995-998, 2020 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-32167747

RESUMO

The recent outbreak of coronavirus infectious disease 2019 (COVID-19) has gripped the world with apprehension and has evoked a scare of epic proportion regarding its potential to spread and infect humans worldwide. As we are in the midst of an ongoing pandemic of COVID-19, scientists are struggling to understand how it resembles and differs from the severe acute respiratory syndrome coronavirus (SARS-CoV) at the genomic and transcriptomic level. In a short time following the outbreak, it has been shown that, similar to SARS-CoV, COVID-19 virus exploits the angiotensin-converting enzyme 2 (ACE2) receptor to gain entry inside the cells. This finding raises the curiosity of investigating the expression of ACE2 in neurological tissue and determining the possible contribution of neurological tissue damage to the morbidity and mortality caused by COIVD-19. Here, we investigate the density of the expression levels of ACE2 in the CNS, the host-virus interaction and relate it to the pathogenesis and complications seen in the recent cases resulting from the COVID-19 outbreak. Also, we debate the need for a model for staging COVID-19 based on neurological tissue involvement.


Assuntos
Sistema Nervoso Central/virologia , Infecções por Coronavirus/fisiopatologia , Interações Hospedeiro-Patógeno , Pneumonia Viral/fisiopatologia , Betacoronavirus/fisiologia , Sistema Nervoso Central/fisiopatologia , Infecções por Coronavirus/imunologia , Humanos , Pandemias , Peptidil Dipeptidase A , Pneumonia Viral/imunologia , Receptores Virais/metabolismo , Distribuição Tecidual
3.
Nihon Yakurigaku Zasshi ; 154(6): 340-344, 2019.
Artigo em Japonês | MEDLINE | ID: mdl-31787687

RESUMO

Central nervous system (CNS) inflammation causes severe neurological dysfunction, such as motor, sensory, and cognitive impairments. One of the reasons for the developing disease depends on the damage of neuronal network, a predominant feature of many CNS diseases. Therefore, protection and/or regeneration of damaged neuronal network after injury is considered to be useful for treating neurological diseases; however, the mechanism of protection and regeneration of neuronal network is not fully elucidated. In this paper, I describe our recent findings about the mechanism that disrupt and regenerate neuronal network by using animal model of multiple sclerosis. I also introduce the key molecules which is involved in inflammation, neurovascular interaction, and systemic regulation. These findings have a potential to contribute develop the new therapies for treating neurological disease.


Assuntos
Doenças do Sistema Nervoso Central/patologia , Sistema Nervoso Central/fisiopatologia , Regeneração Nervosa , Animais , Humanos , Inflamação/patologia , Esclerose Múltipla , Neurônios/patologia
4.
Adv Exp Med Biol ; 1190: 217-247, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31760647

RESUMO

Multiple sclerosis (MS) is an inflammatory demyelinating disorder. Although all MS patients initially show a relapsing-remitting course, 20-50% subsequently enter a chronic progressive course at 10-20 years after onset that greatly influences their activities of daily living. There are 2.5 million MS patients worldwide with large regional and racial differences. In particular, there are many MS patients among Caucasians living in Europe, while the disease is relatively rare in Asians and Africans.Although MS is regarded as an autoimmune disease, many factors such as genetic background, environmental factors, and sex are involved in its pathogenesis. While the immunological mechanisms remain to be fully elucidated, invasion of autoreactive T cells into the central nervous system (CNS) tissue is considered the first step of the disease. These T cells react with myelin antigens and initiate demyelination of the CNS by activating cytotoxic T cells, macrophages, and B cells through the release of inflammatory cytokines. As a treatment option, disease-modifying therapies have recently been developed to prevent the recurrence of MS in addition to conventional treatment with corticosteroids for acute relapse. However, there are still few effective treatments for the chronic progressive phase, and it is thus imperative to decipher the mechanism for chronic progression.


Assuntos
Esclerose Múltipla/fisiopatologia , Linfócitos T/imunologia , Atividades Cotidianas , Linfócitos B/imunologia , Sistema Nervoso Central/fisiopatologia , Citocinas/imunologia , Humanos , Macrófagos/imunologia , Esclerose Múltipla/imunologia , Bainha de Mielina/imunologia
5.
Rinsho Ketsueki ; 60(9): 1212-1220, 2019.
Artigo em Japonês | MEDLINE | ID: mdl-31597846

RESUMO

It is well known that acute lymphoblastic leukemia (ALL) cells can invade the central nervous system (CNS), but the underlying mechanism of such invasion is still unclear. We discovered the direct routes taken by ALL cells when migrating into CNS in ALL model mice. We observed that ALL cells migrate along the external surface of vessels that pass directly between the vertebral or calvarial bone marrow and the subarachnoid space. The basement membrane of these bridging vessels is enriched in laminin. The laminin is recognized by integrin α6, which is expressed by ALL cells. The interaction between integrin α6 and laminin mediated the invasion of ALL cells. Furthermore, the expression of integrin α6 depends on PI3Kδ activity. Mice with ALL xenografts were treated with a PI3Kδ inhibitor, which decreased integrin α6 expression on ALL cells. This resulted in significant reductions in blast counts in the cerebrospinal fluid and in CNS disease symptoms. Our data suggest that the PI3Kδ inhibitor has potential to prevent CNS involvement in ALL.


Assuntos
Sistema Nervoso Central/fisiopatologia , Classe I de Fosfatidilinositol 3-Quinases/antagonistas & inibidores , Integrina alfa6/metabolismo , Laminina/metabolismo , Leucemia-Linfoma Linfoblástico de Células Precursoras/fisiopatologia , Animais , Membrana Basal , Medula Óssea , Camundongos , Espaço Subaracnóideo , Ensaios Antitumorais Modelo de Xenoenxerto
6.
Mol Biol (Mosk) ; 53(5): 790-798, 2019.
Artigo em Russo | MEDLINE | ID: mdl-31661478

RESUMO

Recently, much attention has been drawn to unraveling the mechanisms of neurodegenerative and neuroinflammatory disease pathogenesis. A special role in the development of neuropathologies is assigned to the interaction of the nervous and the immune systems. Microglia are the cells of the immune system that function as resident macrophages of the central nervous system (CNS) and are involved in the development of CNS, as well as in homeostatic interactions. Impaired microglia can contribute to neuroinflammation and neurodegeneration. With the help of genome editing technologies, the main paradigms in the development and functions of microglia have been addressed. At the same time, an understanding of the mechanisms of regulation of microglia in normal and pathological conditions is necessary to create an effective therapy aimed at treating various neurological diseases. This review focuses on recent findings on the origin of microglia, its regulatory role in the central nervous system, as well as its contribution to the development of neuroinflammation.


Assuntos
Sistema Nervoso Central/citologia , Sistema Nervoso Central/fisiologia , Homeostase , Inflamação/patologia , Microglia/fisiologia , Doenças Neurodegenerativas/patologia , Sistema Nervoso Central/patologia , Sistema Nervoso Central/fisiopatologia , Humanos , Inflamação/fisiopatologia , Microglia/citologia , Microglia/patologia , Doenças Neurodegenerativas/fisiopatologia
7.
Adv Exp Med Biol ; 1161: 193-217, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31562631

RESUMO

Headache is a common complaint after mild traumatic brain injury (mTBI). Changes in the CNS lipidome were previously associated with acrolein-induced headache in rodents. mTBI caused similar headache-like symptoms in rats; therefore, we tested the hypothesis that mTBI might likewise alter the lipidome. Using a stereotaxic impactor, rats were given either a single mTBI or a series of 4 mTBIs 48 h apart. 72 h later for single mTBI and 7 days later for repeated mTBI, the trigeminal ganglia (TG), trigeminal nucleus (TNC), and cerebellum (CER) were isolated. Using HPLC/MS/MS, ~80 lipids were measured in each tissue and compared to sham controls. mTBI drove widespread alterations in lipid levels. Single mTBI increased arachidonic acid and repeated mTBI increased prostaglandins in all 3 tissue types. mTBI affected multiple TRPV agonists, including N-arachidonoyl ethanolamine (AEA), which increased in the TNC and CER after single mTBI. After repeated mTBI, AEA increased in the TG, but decreased in the TNC. Common to all tissue types in single and repeated mTBI was an increase the AEA metabolite, N-arachidonoyl glycine, a potent activator of microglial migration. Changes in the CNS lipidome associated with mTBI likely play a role in headache and in long-term neurodegenerative effects of repeated mTBI.


Assuntos
Lesões Encefálicas Traumáticas , Sistema Nervoso Central , Cefaleia , Inflamação , Lipídeos , Neoplasias , Animais , Lesões Encefálicas Traumáticas/fisiopatologia , Sistema Nervoso Central/fisiopatologia , Cefaleia/fisiopatologia , Inflamação/fisiopatologia , Lipídeos/química , Lipídeos/genética , Lipídeos/fisiologia , Neoplasias/fisiopatologia , Ratos
8.
Trials ; 20(1): 498, 2019 Aug 13.
Artigo em Inglês | MEDLINE | ID: mdl-31409380

RESUMO

BACKGROUND: Frozen shoulder (FS) is a musculoskeletal condition of poorly understood etiology that results in shoulder pain and large mobility deficits. Despite some physical therapy interventions, such as joint mobilization and exercise, having shown therapeutic benefit, a definitive treatment does not currently exist. The aim of this study will be to compare the effectiveness of a central nervous system (CNS)-directed treatment program versus a standard medical and physical therapy care program on outcomes in participants with FS. METHODS/DESIGN: The study is a two-group, randomized clinical trial with blinding of participants and assessors. Participants will be recruited via referrals from orthopedic surgeons and physical therapists, community-based advertisements, private care practices and hospitals. Participants will be randomized to receive either a CNS-focused treatment program or standard medical and physical therapy care. The Shoulder Pain And Disability Index (SPADI) will be the primary outcome, while the Numeric Pain Rating Scale (NPRS), shoulder range of movement (ROM), The Patient Specific Functional Scale, two-point discrimination threshold and laterality judgement accuracy will be the secondary outcomes. Assessment will occur at baseline, at the end of the treatment program (week 10), and at 3 and 6 months' follow-up. DISCUSSION: Preliminary data suggest that treatments that target CNS function are a promising approach to the treatment of people with shoulder pain including patients with FS. In the context of modest effects from most available physical therapy treatments for FS, this CNS-focused approach may lead to improved clinical outcomes. The trial should determine if the CNS-directed program is more effective than traditional interventions at reducing pain intensity and improving function in a FS cohort and will follow up participants for 6 months, providing important information on the persistence of any treatment effects. TRIAL REGISTRATION: NCT03320200 . Registered on October 25, 2017.


Assuntos
Bursite/terapia , Sistema Nervoso Central/fisiopatologia , Modalidades de Fisioterapia , Sensação , Articulação do Ombro/inervação , Bursite/diagnóstico , Bursite/fisiopatologia , Avaliação da Deficiência , Retroalimentação Sensorial , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Amplitude de Movimento Articular , Recuperação de Função Fisiológica , Espanha , Fatores de Tempo , Resultado do Tratamento
9.
Int J Mol Sci ; 20(17)2019 Aug 23.
Artigo em Inglês | MEDLINE | ID: mdl-31450727

RESUMO

The abnormal deposition of proteins in brain tissue is a common feature of neurodegenerative diseases (NDs) often accompanied by the spread of mutated proteins, causing neuronal toxicity. Exosomes play a fundamental role on their releasing in extracellular space after endosomal pathway activation, allowing to remove protein aggregates by lysosomal degradation or their inclusion into multivesicular bodies (MVBs), besides promoting cellular cross-talk. The emerging evidence of pathogenic mutations associated to ND susceptibility, leading to impairment of exosome production and secretion, opens a new perspective on the mechanisms involved in neurodegeneration. Recent findings suggest to investigate the genetic mechanisms regulating the different exosome functions in central nervous system (CNS), to understand their role in the pathogenesis of NDs, addressing the identification of diagnostic and pharmacological targets. This review aims to summarize the mechanisms underlying exosome biogenesis, their molecular composition and functions in CNS, with a specific focus on the recent findings invoking a defective exosome biogenesis as a common biological feature of the major NDs, caused by genetic alterations. Further definition of the consequences of specific genetic mutations on exosome biogenesis and release will improve diagnostic and pharmacological studies in NDs.


Assuntos
Suscetibilidade a Doenças , Exossomos/metabolismo , Variação Genética , Doenças Neurodegenerativas/genética , Doenças Neurodegenerativas/metabolismo , Animais , Biomarcadores , Sistema Nervoso Central/metabolismo , Sistema Nervoso Central/fisiopatologia , Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo , Vesículas Extracelulares/metabolismo , Humanos , Doenças Neurodegenerativas/patologia
10.
PLoS One ; 14(7): e0219674, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31295326

RESUMO

Deprivation of maternal care via lack of somatosensory input causes offspring to experience adverse consequences, especially in the central nervous system. However, little is known about the developmental effect of maternal care on peripheral tissues such as the skin, which includes cutaneous sensory neurons. In the present study, we examined the involvement of maternal care in the development of the skin. We investigated offspring reared by early-weaned mother mice who spontaneously showed lower frequency of licking/grooming on nursing. Offspring of early-weaned mothers showed higher resistance against skin barrier disruption than did offspring of normally-weaned mothers, and had normal skin barrier function in the intact trunk skin. In the dorsal root ganglion of early-weaned mother offspring, we also found up-regulation of mRNA levels of the Mas-related G-protein coupled receptor B4 (MrgprB4), which is a marker of sensory neurons that detect gentle stroking. We further found that levels of MrgprB4 mRNA were correlated with the enhancement of skin resistance. The present findings suggest that maternal somatosensory inputs have a developmental impact on the cutaneous sensory neurons of the skin in offspring. Interestingly, the present results suggest that lower maternal care has a benefit on the skin resistance. This provides important information for understanding the development of peripheral tissues in offspring reared under severe conditions such as lower maternal care in the wild.


Assuntos
Sistema Nervoso Central/fisiopatologia , Asseio Animal/fisiologia , Comportamento Materno/fisiologia , Receptores Acoplados a Proteínas-G/genética , Animais , Comportamento Animal/fisiologia , Sistema Nervoso Central/metabolismo , Gânglios Espinais/metabolismo , Gânglios Espinais/patologia , Humanos , Camundongos , Células Receptoras Sensoriais/metabolismo , Células Receptoras Sensoriais/patologia , Pele/metabolismo , Pele/fisiopatologia , Desmame
11.
Nutrients ; 11(7)2019 Jul 05.
Artigo em Inglês | MEDLINE | ID: mdl-31284389

RESUMO

Multiple sclerosis (MS) is a complex disease of the central nervous system (CNS). The etiology of this multifactorial disease has not been clearly defined. Conventional medical treatment of MS has progressed, but is still based on symptomatic treatment. One of the key factors in the pathogenesis of MS is oxidative stress, enhancing inflammation and neurodegeneration. In MS, both reactive oxygen and nitrogen species are formed in the CNS mainly by activated macrophages and microglia structures, which can lead to demyelination and axon disruption. The course of MS is associated with the secretion of many inflammatory and oxidative stress mediators, including cytokines (IL-1b, IL-6, IL-17, TNF-α, INF-γ) and chemokines (MIP-1a, MCP-1, IP10). The early stage of MS (RRMS) lasts about 10 years, and is dominated by inflammatory processes, whereas the chronic stage is associated with neurodegenerative axon and neuron loss. Since oxidative damage has been known to be involved in inflammatory and autoimmune-mediated processes, antioxidant therapy could contribute to the reduction or even prevention of the progression of MS. Further research is needed in order to establish new aims for novel treatment and provide possible benefits to MS patients. The present review examines the roles of oxidative stress and non-pharmacological anti-oxidative therapies in MS.


Assuntos
Antioxidantes/uso terapêutico , Sistema Nervoso Central/efeitos dos fármacos , Esclerose Múltipla/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Animais , Anti-Inflamatórios/uso terapêutico , Antioxidantes/efeitos adversos , Sistema Nervoso Central/metabolismo , Sistema Nervoso Central/fisiopatologia , Citocinas/metabolismo , Humanos , Mediadores da Inflamação/metabolismo , Esclerose Múltipla/dietoterapia , Esclerose Múltipla/metabolismo , Esclerose Múltipla/fisiopatologia , Estado Nutricional , Transdução de Sinais , Resultado do Tratamento
12.
Nat Rev Neurol ; 15(8): 447-458, 2019 08.
Artigo em Inglês | MEDLINE | ID: mdl-31256193

RESUMO

Microglia are resident macrophages of the CNS that are involved in its development, homeostasis and response to infection and damage. Microglial activation is a common feature of neurological disorders, and although in some instances this activation can be damaging, protective and regenerative functions of microglia have been revealed. The most prominent example of the regenerative functions is a role for microglia in supporting regeneration of myelin after injury, a process that is critical for axonal health and relevant to numerous disorders in which loss of myelin integrity is a prevalent feature, such as multiple sclerosis, Alzheimer disease and motor neuron disease. Although drugs that are intended to promote remyelination are entering clinical trials, the mechanisms by which remyelination is controlled and how microglia are involved are not completely understood. In this Review, we discuss work that has identified novel regulators of microglial activation - including molecular drivers, population heterogeneity and turnover - that might influence their pro-remyelination capacity. We also discuss therapeutic targeting of microglia as a potential approach to promoting remyelination.


Assuntos
Sistema Nervoso Central/fisiologia , Doenças Desmielinizantes/fisiopatologia , Microglia/fisiologia , Remielinização , Envelhecimento , Animais , Sistema Nervoso Central/fisiopatologia , Doenças Desmielinizantes/terapia , Homeostase , Humanos , Ativação de Macrófagos
14.
PLoS One ; 14(6): e0217985, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31216311

RESUMO

OBJECTIVE: Segmented deep brain stimulation leads in the subthalamic nucleus have shown to increase therapeutic window using directional stimulation. However, it is not fully understood how these segmented leads with reduced electrode size modify the volume of tissue activated (VTA) and how this in turn relates with clinically observed therapeutic and side effect currents. Here, we investigated the differences between directional and omnidirectional stimulation and associated VTAs with patient-specific therapeutic and side effect currents for the two stimulation modes. APPROACH: Nine patients with Parkinson's disease underwent DBS implantation in the subthalamic nucleus. Therapeutic and side effect currents were identified intraoperatively with a segmented lead using directional and omnidirectional stimulation (these current thresholds were assessed in a blinded fashion). The electric field around the lead was simulated with a finite-element model for a range of stimulation currents for both stimulation modes. VTAs were estimated from the electric field by numerical differentiation and thresholding. Then for each patient, the VTAs for given therapeutic and side effect currents were projected onto the patient-specific subthalamic nucleus and lead position. RESULTS: Stimulation with segmented leads with reduced electrode size was associated with a significant reduction of VTA and a significant increase of radial distance in the best direction of stimulation. While beneficial effects were associated with activation volumes confined within the anatomical boundaries of the subthalamic nucleus at therapeutic currents, side effects were associated with activation volumes spreading beyond the nucleus' boundaries. SIGNIFICANCE: The clinical benefits of segmented leads are likely to be obtained by a VTA confined within the subthalamic nucleus and a larger radial distance in the best stimulation direction, while steering the VTA away from unwanted fiber tracts outside the nucleus. Applying the same concepts at a larger scale and in chronically implanted patients may help to predict the best stimulation area.


Assuntos
Estimulação Encefálica Profunda/métodos , Doença de Parkinson/terapia , Núcleo Subtalâmico/efeitos da radiação , Adulto , Idoso , Sistema Nervoso Central/fisiopatologia , Sistema Nervoso Central/efeitos da radiação , Estimulação Encefálica Profunda/efeitos adversos , Estimulação Elétrica , Eletrodos Implantados , Campos Eletromagnéticos/efeitos adversos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Contração Muscular/efeitos da radiação , Doença de Parkinson/fisiopatologia , Núcleo Subtalâmico/fisiopatologia
15.
Acta Biochim Biophys Sin (Shanghai) ; 51(6): 555-561, 2019 Jun 20.
Artigo em Inglês | MEDLINE | ID: mdl-31056639

RESUMO

Neuropathic pain is caused by the damage or dysfunction of the nervous system. In many neuropathic pain models, there is an increase in the number of gap junction (GJ) channels, especially the upregulation of the expression of connexin43 (Cx43), leading to the secretion of various types of cytokines and involvement in the formation of neuropathic pain. GJs are widely distributed in mammalian organs and tissues, and Cx43 is the most abundant connexin (Cx) in mammals. Astrocytes are the most abundant glial cell type in the central nervous system (CNS), which mainly express Cx43. More importantly, GJs play an important role in regulating cell metabolism, signaling, and function. Many existing literatures showed that Cx43 plays an important role in the nervous system, especially in the CNS under normal and pathological conditions. However, many internal mechanisms have not yet been thoroughly explored. In this review, we summarized the current understanding of the role and association of Cx and pannexin channels in neuropathic pain, especially after spinal cord injury, as well as some of our own insights and thoughts which suggest that Cx43 may become an emerging therapeutic target for future neuropathic pain, bringing new hope to patients.


Assuntos
Astrócitos/efeitos dos fármacos , Conexina 43/metabolismo , Neuralgia/metabolismo , Traumatismos da Medula Espinal/metabolismo , Animais , Astrócitos/metabolismo , Carbenoxolona/uso terapêutico , Sistema Nervoso Central/efeitos dos fármacos , Sistema Nervoso Central/metabolismo , Sistema Nervoso Central/fisiopatologia , Conexina 43/antagonistas & inibidores , Junções Comunicantes/efeitos dos fármacos , Junções Comunicantes/metabolismo , Humanos , Terapia de Alvo Molecular/métodos , Neuralgia/fisiopatologia , Neuralgia/prevenção & controle , Traumatismos da Medula Espinal/tratamento farmacológico , Traumatismos da Medula Espinal/fisiopatologia
16.
Internist (Berl) ; 60(7): 690-700, 2019 Jul.
Artigo em Alemão | MEDLINE | ID: mdl-31093686

RESUMO

Treatments in oncology, transplantation medicine and immunology frequently lead to immunodeficiency. This review presents the most important opportunistic neurologic infections, mostly of the central nervous system (CNS). Signs and symptoms, diagnostic procedures and therapeutic options are presented. The most frequent infections are due to varicella zoster virus (VZV), Cryptococcus neoformans and Toxoplasma gondii; JC virus (JCV) and cytomegalovirus (CMV) are rare causes of encephalitis. Differential diagnoses include infection by non-opportunistic causatives, therapy associated neurotoxicity, Epstein-Barr virus (EBV) associated CNS lymphoma, recurrence of the malignancy, as well as non-infectious diseases like intracranial bleeding, ischemic stroke, autoimmune diseases and posterior reversible leukencephalopathy syndrome. Treatment of these patients, moreover, needs to consider all previous therapies and to involve a neurologist.


Assuntos
Sistema Nervoso Central/fisiopatologia , Criptococose , Hospedeiro Imunocomprometido , Infecções Oportunistas/complicações , Toxoplasmose , Infecção pelo Vírus da Varicela-Zoster , Doenças do Sistema Nervoso Central/etiologia , Criptococose/diagnóstico , Criptococose/etiologia , Cryptococcus neoformans/isolamento & purificação , Encefalite/etiologia , Herpes Simples/etiologia , Herpesvirus Humano 3/isolamento & purificação , Humanos , Leucoencefalopatia Multifocal Progressiva/etiologia , Infecções Oportunistas/diagnóstico , Infecções Oportunistas/virologia , Toxoplasma , Toxoplasmose/diagnóstico , Toxoplasmose/etiologia , Infecção pelo Vírus da Varicela-Zoster/diagnóstico , Infecção pelo Vírus da Varicela-Zoster/virologia
17.
Pharmacol Biochem Behav ; 182: 22-34, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-31103523

RESUMO

Attention Deficit Hyperactivity Disorder (ADHD) is a persistent, and impairing pediatric-onset neurodevelopmental condition. Its high prevalence, and recurrent controversy over its widespread identification and treatment, drive strong interest in its etiology and mechanisms. Emerging evidence for a role for neuroinflammation in ADHD pathophysiology is of great interest. This evidence includes 1) the above-chance comorbidity of ADHD with inflammatory and autoimmune disorders, 2) initial studies indicating an association with ADHD and increased serum cytokines, 3) preliminary evidence from genetic studies demonstrating associations between polymorphisms in genes associated with inflammatory pathways and ADHD, 4) emerging evidence that early life exposure to environmental factors may increase risk for ADHD via an inflammatory mechanism, and 5) mechanistic evidence from animal models of maternal immune activation documenting behavioral and neural outcomes consistent with ADHD. Prenatal exposure to inflammation is associated with changes in offspring brain development including reductions in cortical gray matter volume and the volume of certain cortical areas -parallel to observations associated with ADHD. Alterations in neurotransmitter systems, including the dopaminergic, serotonergic and glutamatergic systems, are observed in ADHD populations. Animal models provide strong evidence that development and function of these neurotransmitters systems are sensitive to exposure to in utero inflammation. In summary, accumulating evidence from human studies and animal models, while still incomplete, support a potential role for neuroinflammation in the pathophysiology of ADHD. Confirmation of this association and the underlying mechanisms have become valuable targets for research. If confirmed, such a picture may be important in opening new intervention routes.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/etiologia , Inflamação/complicações , Adolescente , Animais , Transtorno do Deficit de Atenção com Hiperatividade/imunologia , Transtorno do Deficit de Atenção com Hiperatividade/metabolismo , Transtorno do Deficit de Atenção com Hiperatividade/fisiopatologia , Sistema Nervoso Central/embriologia , Sistema Nervoso Central/crescimento & desenvolvimento , Sistema Nervoso Central/fisiopatologia , Criança , Citocinas/metabolismo , Dopamina/metabolismo , Feminino , Ácido Glutâmico/metabolismo , Humanos , Inflamação/imunologia , Inflamação/metabolismo , Masculino , Camundongos , Modelos Animais , Norepinefrina/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal , Fatores de Risco , Serotonina/metabolismo , Adulto Jovem , Ácido gama-Aminobutírico/metabolismo
18.
Biomed Res Int ; 2019: 8930904, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31032365

RESUMO

Objectives: To analyze the central auditory nervous system function through behavioral and electrophysiological tests in children with a history of otitis media and subsequent bilateral tubes placement surgery. Methods: The participants were divided into two groups between eight and 14 years old: control group (CG) consisted of 40 children with no history of otitis media; experimental group (EG) consisted of 50 children with documented history of otitis media and undertook a surgery for bilateral tubes placement. All children completed audiological evaluation (audiometry, speech audiometry, and immittance audiometry), behavioral evaluation (tests: dichotic digits, synthetic sentence identification with ipsilateral competing message, gaps-in-noise, frequency pattern), and electrophysiological evaluation (Auditory Brainstem Response, ABR, Frequency Following Response, FFR (verbal), and Long Latency Auditory Evoked Potential, LLAEP). Results: The EG group showed significantly poorer performance (p<0.001) than the CG for all auditory abilities studied. The results revealed significant latency delays and reduced amplitude (p<0.05) of waves III and V for ABR; significant latency delay was seen of potentials P2, N2, and P300 for LLAEP; significant latency delays and reduced amplitude (p<0.05) were observed for FFR in children with a history of otitis media. Conclusion: The results demonstrate negative effect of otitis media in the auditory abilities and electrophysiological measures in children with a history of otitis media.


Assuntos
Doenças do Sistema Nervoso Autônomo/fisiopatologia , Sistema Nervoso Central/fisiopatologia , Transtornos do Desenvolvimento da Linguagem/fisiopatologia , Otite Média/fisiopatologia , Adolescente , Audiometria de Tons Puros , Audiometria da Fala , Doenças do Sistema Nervoso Autônomo/etiologia , Doenças do Sistema Nervoso Autônomo/cirurgia , Criança , Tuba Auditiva/fisiopatologia , Tuba Auditiva/cirurgia , Potenciais Evocados Auditivos , Potenciais Evocados Auditivos do Tronco Encefálico/fisiologia , Feminino , Humanos , Transtornos do Desenvolvimento da Linguagem/etiologia , Transtornos do Desenvolvimento da Linguagem/cirurgia , Masculino , Otite Média/complicações , Otite Média/cirurgia
19.
PLoS One ; 14(4): e0213528, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30969973

RESUMO

Locked-in syndrome (LIS) is a state of quadriplegia and anarthria with preserved consciousness, which is generally triggered by a disruption of specific white matter fiber tracts, following a lesion in the ventral part of the pons. However, the impact of focal lesions on the whole brain white matter microstructure and structural connectivity pathways remains unknown. We used diffusion tensor magnetic resonance imaging (DT-MRI) and tract-based statistics to characterise the whole white matter tracts in seven consecutive LIS patients, with ventral pontine injuries but no significant supratentorial lesions detected with morphological MRI. The imaging was performed in the acute phase of the disease (26 ± 13 days after the accident). DT-MRI-derived metrics were used to quantitatively assess global white matter alterations. All diffusion coefficient Z-scores were decreased for almost all fiber tracts in all LIS patients, with diffuse white matter alterations in both infratentorial and supratentorial areas. A mixture model of two multidimensional Gaussian distributions was fitted to cluster the white matter fiber tracts studied in two groups: the least (group 1) and most injured white matter fiber tracts (group 2). The greatest injuries were revealed along pathways crossing the lesion responsible for the LIS: left and right medial lemniscus (98.4% and 97.9% probability of belonging to group 2, respectively), left and right superior cerebellar peduncles (69.3% and 45.7% probability) and left and right corticospinal tract (20.6% and 46.5% probability). This approach demonstrated globally compromised white matter tracts in the acute phase of LIS, potentially underlying cognitive deficits.


Assuntos
Tronco Encefálico/diagnóstico por imagem , Imagem de Tensor de Difusão , Substância Branca/diagnóstico por imagem , Adulto , Idoso , Vias Auditivas/diagnóstico por imagem , Vias Auditivas/fisiopatologia , Lesões Encefálicas/diagnóstico , Lesões Encefálicas/diagnóstico por imagem , Lesões Encefálicas/fisiopatologia , Tronco Encefálico/fisiopatologia , Sistema Nervoso Central/diagnóstico por imagem , Sistema Nervoso Central/fisiopatologia , Transtornos Cognitivos/diagnóstico , Transtornos Cognitivos/diagnóstico por imagem , Transtornos Cognitivos/fisiopatologia , Feminino , Humanos , /fisiopatologia , Masculino , Pessoa de Meia-Idade , Distribuição Normal , Tratos Piramidais/diagnóstico por imagem , Tratos Piramidais/fisiopatologia , Substância Branca/lesões , Substância Branca/fisiopatologia
20.
Acta Cytol ; 63(3): 224-232, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30982032

RESUMO

OBJECTIVE: Intraoperative examination is a highly valuable tool for the evaluation of central nervous system (CNS) lesions, helping the neurosurgeon to determine the best surgical management. This study aimed to evaluate the accuracy and to analyze the diagnostic disagreements and pitfalls of the intraoperative examinations through correlation with the final histopathological diagnosis in CNS lesions. STUDY DESIGN: Retrospective analysis of intraoperative examination of CNS lesions and their final diagnosis obtained during 16 consecutive years. All diagnoses were reviewed and classified according to World Health Organization (WHO) grading for CNS tumors. Squash was performed in 119 cases, while frozen section and both methods were done in 7 cases each. RESULTS: Among the 133 intraoperative examinations considered, 114 (85.7%) presented concordance and 19 (14.3%) diagnostic disagreement when compared with subsequent histopathological examinations. The sensitivity and specificity for the detection of neoplasia in intraoperative examination was 98 and 94%, respectively. The positive and negative predictive values were 99 and 88%, respectively. The accuracy for neoplastic and nonneoplastic disease was 85.7%. Disagreements were more frequent among low-grade (WHO grades I and II) neoplasms and nonmalignant cases. CONCLUSIONS: Our results showed good accuracy of the intraoperative assessments for diagnosis of CNS lesions, particularly in high-grade (grades III and IV) lesions and metastatic neoplasms.


Assuntos
Doenças do Sistema Nervoso Central/diagnóstico , Neoplasias do Sistema Nervoso Central/diagnóstico , Sistema Nervoso Central/patologia , Monitorização Neurofisiológica Intraoperatória/métodos , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Sistema Nervoso Central/fisiopatologia , Sistema Nervoso Central/cirurgia , Doenças do Sistema Nervoso Central/fisiopatologia , Doenças do Sistema Nervoso Central/cirurgia , Neoplasias do Sistema Nervoso Central/fisiopatologia , Neoplasias do Sistema Nervoso Central/cirurgia , Criança , Pré-Escolar , Citodiagnóstico/métodos , Feminino , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Sensibilidade e Especificidade , Adulto Jovem
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