Página 1 dos resultados de 139 itens digitais encontrados em 0.031 segundos

Efeitos da exposição ao etanol em camundongos adolescentes e adultos: comportamentos relacionados à recompensa, sensibilização comportamental e o papel dos sistemas dopaminérgico e glutamatérgico.; Effects of ethanol exposure in adolescent and adult mice: behaviors related to reward, behavioral sensitization and the role of the dopaminergic and glutamatergic systems.

Nascimento, Priscila Fernandes Carrara do
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 16/09/2011 PT
Relevância na Pesquisa
45.82%
O uso de drogas de abuso inicia-se principalmente na adolescência, um período em que o sistema nervoso central está passando por mudanças maturacionais neuroquímicas e neuroanatômicas. Assim, o objetivo desse projeto foi avaliar efeitos comportamentais e neuroquímicos da exposição ao etanol em camundongos adolescentes e adultos. O presente projeto investigou: o desenvolvimento da sensibilização comportamental ao etanol em camundongos adolescentes e adultos; possíveis alterações na sinalização dopaminérgica e glutamatérgica no núcleo accumbens e estriado de camundongos sensibilizados ao etanol durante a adolescência; participação da via AMPc/PKA na sensibilização comportamental ao etanol em camundongos adolescentes e adultos; efeitos reforçadores do etanol em camundongos adolescentes e adultos por meio do modelo de auto-administração; efeitos reforçadores do etanol utilizando-se o aparelho de preferência condicionada de lugar, que possibilita a quantificação do tempo de permanência do animal no ambiente associado aos efeitos da droga; efeito de intoxicações crônicas seguidas de abstinência no padrão de consumo.; The use of drugs of abuse begins mainly in adolescence, a period in which the central nervous system is undergoing neurochemical and neuroanatomical maturation changes. Thus...

Avaliação somatossensorial do sistema trigeminal em condições dolorosas crônicas: testes quantitativos sensoriais e limiar de percepção atual; Trigeminal system somatosensory evaluation in chronic pain patients: quantitative sensory tests and current perception threshold

Sydney, Priscila Brenner Hilgenberg
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 20/05/2013 PT
Relevância na Pesquisa
65.87%
A dor crônica envolve complexos processos de gênese e condução neural e é decorrente da ativação de mecanismos periféricos e centrais de manutenção. Muitos pacientes crônicos são refratários aos diferentes tipos de tratamento propostos, o que gera a suspeita de que de alguma maneira estes não estão sendo totalmente eficazes. O objetivo deste trabalho é avaliar os mecanismos de condução, manutenção e modulação da dor em diferentes condições dolorosas crônicas. Foram avaliadas 92 mulheres, divididas em 5 grupos: Grupo I, 20 pacientes com Dor Miofascial da musculatura mastigatória; Grupo II, 20 pacientes com Fibromialgia; Grupo III, 20 pacientes com Cefaleia Crônica Diária; Grupo IV, 12 pacientes com Neuralgia Trigeminal e Grupo V, 20 pacientes saudáveis assintomáticas. Foram aplicados dois questionários, o IDATE e o OHIP-30, para mensuração do estado ansioso e da qualidade de vida relacionada a condição dolorosa diagnosticada, respectivamente. Todas as pacientes foram submetidas a Testes Quantitativos Sensoriais, como: Limiar de Dor à Pressão, Limiar de Detecção Mecânico, Limiar Doloroso Mecânico, Tolerância à Dor Isquêmica, Sensibilidade Dolorosa ao Frio, Sensação Pós-Estímulo e Controle da Modulação da Dor. Além disso...

Dor: aspectos atuais da sensibilização periférica e central

Rocha, Anita Perpétua Carvalho; Kraychete, Durval Campos; Lemonica, Lino; Carvalho, Lídia Raquel de; Barros, Guilherme Antônio Moreira de; Garcia, João Batista dos Santos; Sakata, Rioko Kimiko
Fonte: Sociedade Brasileira de Anestesiologia Publicador: Sociedade Brasileira de Anestesiologia
Tipo: Artigo de Revista Científica Formato: 94-105
POR
Relevância na Pesquisa
46.04%
JUSTIFICATIVA E OBJETIVOS: As pesquisas recentes têm focalizado a plasticidade bioquímica e estrutural do sistema nervoso decorrente da lesão tissular. Os mecanismos envolvidos na transição da dor aguda para crônica são complexos e envolvem a interação de sistemas receptores e o fluxo de íons intracelulares, sistemas de segundo mensageiro e novas conexões sinápticas. O objetivo deste artigo foi discutir os novos mecanismos que envolvem a sensibilização periférica e central. CONTEÚDO: A lesão tissular provoca aumento na resposta dos nociceptores, chamada de sensibilização ou facilitação. Esses fenômenos iniciam-se após a liberação local de mediadores inflamatórios e a ativação de células do sistema imune ou de receptores específicos no sistema nervoso periférico e central. CONCLUSÕES: As lesões do tecido e dos neurônios resultam em sensibilização de nociceptores e facilitação da condução nervosa central e periférica.; JUSTIFICATIVA Y OBJETIVOS: Las recientes investigaciones se han centrado en la plasticidad bioquímica y estructural del sistema nervioso proveniente de la lesión tisular. Los mecanismos involucrados en transición del dolor agudo para crónico son complejos e involucran la interacción de sistemas receptores y el flujo de iones intracelulares...

Intrinsic responses to Borna disease virus infection of the central nervous system

Morimoto, Kinjiro; Hooper, D. Craig; Bornhorst, Annette; Corisdeo, Susanne; Bette, Michael; Fu, Zhen Fang; Schäfer, Martin K.-H.; Koprowski, Hilary; Weihe, Eberhard; Dietzschold, Bernhard
Fonte: The National Academy of Sciences of the USA Publicador: The National Academy of Sciences of the USA
Tipo: Artigo de Revista Científica
Publicado em 12/11/1996 EN
Relevância na Pesquisa
65.8%
Immune cells invading the central nervous system (CNS) in response to Borna disease virus (BDV) antigens are central to the pathogenesis of Borna disease (BD). We speculate that the response of the resident cells of the brain to infection may be involved in the sensitization and recruitment of these inflammatory cells. To separate the responses of resident cells from those of cells infiltrating from the periphery, we used dexamethasone to inhibit inflammatory reactions in BD. Treatment with dexamethasone prevented the development of clinical signs of BD, and the brains of treated animals showed no neuropathological lesions and a virtual absence of markers of inflammation, cell infiltration, or activation normally seen in the CNS of BDV-infected rats. In contrast, treatment with dexamethasone exacerbated the expression of BDV RNA, which was paralleled by a similarly elevated expression of mRNAs for egr-1, c-fos, and c-jun. Furthermore, dexamethasone failed to inhibit the increase in expression of mRNAs for tumor necrosis factor α, macrophage inflammatory protein 1β, interleukin 6, and mob-1, which occurs in the CNS of animals infected with BDV. Our findings suggest that these genes, encoding transcription factors...

Pharmacological modulation of pain-related brain activity during normal and central sensitization states in humans

Iannetti, G. D.; Zambreanu, L.; Wise, R. G.; Buchanan, T. J.; Huggins, J. P.; Smart, T. S.; Vennart, W.; Tracey, I.
Fonte: National Academy of Sciences Publicador: National Academy of Sciences
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
45.96%
Abnormal processing of somatosensory inputs in the central nervous system (central sensitization) is the mechanism accounting for the enhanced pain sensitivity in the skin surrounding tissue injury (secondary hyperalgesia). Secondary hyperalgesia shares clinical characteristics with neurogenic hyperalgesia in patients with neuropathic pain. Abnormal brain responses to somatosensory stimuli have been found in patients with hyperalgesia as well as in normal subjects during experimental central sensitization. The aim of this study was to assess the effects of gabapentin, a drug effective in neuropathic pain patients, on brain processing of nociceptive information in normal and central sensitization states. Using functional magnetic resonance imaging (fMRI) in normal volunteers, we studied the gabapentin-induced modulation of brain activity in response to nociceptive mechanical stimulation of normal skin and capsaicin-induced secondary hyperalgesia. The dose of gabapentin was 1,800 mg per os, in a single administration. We found that (i) gabapentin reduced the activations in the bilateral operculoinsular cortex, independently of the presence of central sensitization; (ii) gabapentin reduced the activation in the brainstem, only during central sensitization; (iii) gabapentin suppressed stimulus-induced deactivations...

Biology and therapy of fibromyalgia: pain in fibromyalgia syndrome

Staud, Roland
Fonte: BioMed Central Publicador: BioMed Central
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
45.92%
Fibromyalgia (FM) pain is frequent in the general population but its pathogenesis is only poorly understood. Many recent studies have emphasized the role of central nervous system pain processing abnormalities in FM, including central sensitization and inadequate pain inhibition. However, increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both. It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain. This mechanism represents a hallmark of FM and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state. Additional factors, including pain related negative affect and poor sleep have been shown to significantly contribute to clinical FM pain. Better understanding of these mechanisms and their relationship to central sensitization and clinical pain will provide new approaches for the prevention and treatment of FM and other chronic pain syndromes.

Integrated defense system overlaps as a disease model: with examples for multiple chemical sensitivity.

Rowat, S C
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /02/1998 EN
Relevância na Pesquisa
45.9%
The central nervous, immune, and endocrine systems communicate through multiple common messengers. Over evolutionary time, what may be termed integrated defense system(s) (IDS) have developed to coordinate these communications for specific contexts; these include the stress response, acute-phase response, nonspecific immune response, immune response to antigen, kindling, tolerance, time-dependent sensitization, neurogenic switching, and traumatic dissociation (TD). These IDSs are described and their overlap is examined. Three models of disease production are generated: damage, in which IDSs function incorrectly; inadequate/inappropriate, in which IDS response is outstripped by a changing context; and evolving/learning, in which the IDS learned response to a context is deemed pathologic. Mechanisms of multiple chemical sensitivity (MCS) are developed from several IDS disease models. Model 1A is pesticide damage to the central nervous system, overlapping with body chemical burdens, TD, and chronic zinc deficiency; model 1B is benzene disruption of interleukin-1, overlapping with childhood developmental windows and hapten-antigenic spreading; and model 1C is autoimmunity to immunoglobulin-G (IgG), overlapping with spreading to other IgG-inducers...

The effects of protein phosphatase inhibitors on the duration of central sensitization of rat dorsal horn neurons following injection of capsaicin

Zhang, Xuan; Wu, Jing; Fang, Li; Willis, William D
Fonte: BioMed Central Publicador: BioMed Central
Tipo: Artigo de Revista Científica
Publicado em 17/07/2006 EN
Relevância na Pesquisa
55.92%
Protein kinases and phosphatases catalyze opposing reactions of phosphorylation and dephosphorylation, which may modulate the function of crucial signaling proteins in central nervous system. This is an important mechanism in the regulation of intracellular signal transduction pathways in nociceptive neurons. To explore the role of protein phosphatase in central sensitization of spinal nociceptive neurons following peripheral noxious stimulation, using electrophysiological recording techniques, we investigated the role of two inhibitors of protein phosphatase type 2A (PP2A), fostriecin and okadaic acid (OA), on the responses of dorsal horn neurons to mechanical stimuli in anesthetized rats following intradermal injection of capsaicin. Central sensitization was initiated by injection of capsaicin into the plantar surface of the left paw. A microdialysis fiber was implanted in the spinal cord dorsal horn for perfusion of ACSF and inhibitors of PP2A, fostriecin and okadaic acid. We found that in ACSF pretreated animals, the responses to innocuous and noxious stimuli following capsaicin injection increased over a period of 15 min after injection and had mostly recovered by 60 min later. However, pre- or post-treatment with the phosphatase inhibitors...

Interrater Reliability of a New Classification System for Patients with Neural Low Back-Related Leg Pain

Schäfer, Axel; Hall, Toby M; Lüdtke, Kerstin; Mallwitz, Joachim; Briffa, Noelle K
Fonte: Journal of Manual & Manipulative Therapy, Inc. Publicador: Journal of Manual & Manipulative Therapy, Inc.
Tipo: Artigo de Revista Científica
Publicado em //2009 EN
Relevância na Pesquisa
45.97%
The aim of this study was to investigate the reliability of a new classification system for low back-related leg pain arising from neural tissue dysfunction. Leg pain is a frequent accompaniment to back pain and is an indicator of the severity and prognosis of the disorder. For optimal patient care, treatment should be directed according to the identified pathophysiological mechanisms. The authors have proposed a sub-classification of neural low back-related leg pain into four categories, each requiring a different management strategy: Central Sensitization (CS), comprising major features of sensitization of the somatosensory system; Denervation (D), arising from significant axonal compromise without evidence of major central nervous system changes; Peripheral Nerve Sensitization (PNS), arising from nerve trunk inflammation without clinical evidence of significant denervation; and Musculoskeletal pain (M), referred from non-neural structures such as the disc or facet joints. The purpose of this study was to investigate the interrater reliability of this classification system. Forty consecutive patients with unilateral low back-related leg pain were independently assessed by five pairs of examiners using a physical examination protocol...

Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity

Latremoliere, Alban; Woolf, Clifford J.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /09/2009 EN
Relevância na Pesquisa
46.11%
Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations.

DNA Methylation Regulates Cocaine-Induced Behavioral Sensitization in Mice

Anier, Kaili; Malinovskaja, Kristina; Aonurm-Helm, Anu; Zharkovsky, Alexander; Kalda, Anti
Fonte: Nature Publishing Group Publicador: Nature Publishing Group
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
45.83%
The behavioral sensitization produced by repeated cocaine treatment represents the neural adaptations underlying some of the features of addiction in humans. Cocaine administrations induce neural adaptations through regulation of gene expression. Several studies suggest that epigenetic modifications, including DNA methylation, are the critical regulators of gene expression in the adult central nervous system. DNA methylation is catalyzed by DNA methyltransferases (DNMTs) and consequent promoter region hypermethylation is associated with transcriptional silencing. In this study a potential role for DNA methylation in a cocaine-induced behavioral sensitization model in mice was explored. We report that acute cocaine treatment caused an upregulation of DNMT3A and DNMT3B gene expression in the nucleus accumbens (NAc). Using methylated DNA immunoprecipitation, DNA bisulfite modification, and chromatin immunoprecipitation assays, we observed that cocaine treatment resulted in DNA hypermethylation and increased binding of methyl CpG binding protein 2 (MeCP2) at the protein phosphatase-1 catalytic subunit (PP1c) promoter. These changes are associated with transcriptional downregulation of PP1c in NAc. In contrast, acute and repeated cocaine administrations induced hypomethylation and decreased binding of MeCP2 at the fosB promoter...

The role of the central nervous system in the generation and maintenance of chronic pain in rheumatoid arthritis, osteoarthritis and fibromyalgia

Lee, Yvonne C; Nassikas, Nicholas J; Clauw, Daniel J
Fonte: BioMed Central Publicador: BioMed Central
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
75.83%
Pain is a key component of most rheumatologic diseases. In fibromyalgia, the importance of central nervous system pain mechanisms (for example, loss of descending analgesic activity and central sensitization) is well documented. A few studies have also noted alterations in central pain processing in osteoarthritis, and some data, including the observation of widespread pain sensitivity, suggest that central pain-processing defects may alter the pain response in rheumatoid arthritis patients. When central pain is identified, different classes of analgesics (for example, serotonin-norepinephrine reuptake inhibitors, α2δ ligands) may be more effective than drugs that treat peripheral or nociceptive pain (for example, nonsteroidal anti-inflammatory drugs and opioids).

Involvement of µ-Opioid Receptor in Methamphetamine-Induced Behavioral Sensitization

Tien, Lu-Tai; Ho, Ing-Kang
Fonte: Bentham Science Publishers Ltd. Publicador: Bentham Science Publishers Ltd.
Tipo: Artigo de Revista Científica
Publicado em /03/2011 EN
Relevância na Pesquisa
46.08%
Methamphetamine is a potent addictive stimulant drug that activates certain systems in the brain. It is a member of the amphetamine family, but the effects of methamphetamine are much more potent, longer lasting, and more harmful to the central nervous system. Repeated administration of methamphetamine induces behavioral sensitization, which is considered to be related to compulsive drug-seeking behavior. Although the mechanism responsible for methamphetamine-induced behavioral sensitization remains unclear, it is believed that the mesolimbic dopaminergic system in the central nervous system plays a critical role in the development of behavioral sensitization. Our previous studies indicate that the involvement of the μ-opioid receptor system underlies the development of methamphetamine-induced behavioral sensitization. Understanding the mechanisms of behavioral sensitization that are regulated by the μ-opioid receptor system would be helpful in developing therapeutic programs against methamphetamine addiction. This review briefly discusses the neural circuitry and cellular mechanisms that are known to play a central role in methamphetamine-induced behavioral sensitization and outlines the role of the μ-opioid receptor system in the development of methamphetamine-induced sensitization.

Dopamine D2 Receptor-Mediated Heterologous Sensitization of AC5 Requires Signalosome Assembly

Ejendal, Karin F. K.; Dessauer, Carmen W.; Hébert, Terence E.; Watts, Val J.
Fonte: Hindawi Publishing Corporation Publicador: Hindawi Publishing Corporation
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
45.86%
Chronic dopamine receptor activation is implicated in several central nervous system disorders. Although acute activation of Gαi-coupled D2 dopamine receptors inhibits adenylyl cyclase, persistent activation enhances adenylyl cyclase activity, a phenomenon called heterologous sensitization. Previous work revealed a requirement for Gαs in D2-induced heterologous sensitization of AC5. To elucidate the mechanism of Gαs dependency, we expressed Gαs mutants in Gαs-deficient GnasE2−/E2− cells. Neither Gαs-palmitoylation nor Gαs-Gβγ interactions were required for sensitization of AC5. Moreover, we found that coexpressing βARKct-CD8 or Sar1(H79G) blocked heterologous sensitization. These studies are consistent with a role for Gαs-AC5 interactions in sensitization however, Gβγ appears to have an indirect role in heterologous sensitization of AC5, possibly by promoting proper signalosome assembly.

THE CENTRAL SENSITIZATION INVENTORY (CSI): ESTABLISHING CLINICALLY-SIGNIFICANT VALUES FOR IDENTIFYING CENTRAL SENSITIVITY SYNDROMES IN AN OUTPATIENT CHRONIC PAIN SAMPLE

Neblett, Randy; Cohen, Howard; Choi, Yunhee; Hartzell, Meredith; Williams, Mark; Mayer, Tom G.; Gatchel, Robert J.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
45.87%
Central Sensitization (CS) is a proposed physiological phenomenon in which central nervous system neurons become hyper-excitable, resulting in hypersensitivity to both noxious and non-noxious stimuli. The term Central Sensitivity Syndrome (CSS) describes a group of medically-indistinct (or nonspecific) disorders, such as fibromyalgia, chronic fatigue, and irritable bowel, for which CS may be a common etiology. In a previous study, the Central Sensitization Inventory (CSI) was introduced as a screening instrument for clinicians to help identify patients with a CSS. It was found to have high reliability and validity (test-retest reliability = 0.82; Cronbach’s alpha = 0.88). The present study investigated a cohort of 121 patients who were referred to a multidisciplinary pain center, which specialized in the assessment and treatment of complex pain and psychophysiological disorders, including CSSs. A large percentage of patients (n = 89, 74%) met clinical criteria for one or more CSSs, and CSI scores were positively correlated with the number of diagnosed CSSs. A Receiver Operating Characteristic (ROC) analysis determined that a CSI score of 40 out of 100 best distinguished between the CSS patient group and a non-patient comparison sample (n = 129) (AUC= 0.86...

Evoked Temporal Summation in Cats to Highlight Central Sensitization Related to Osteoarthritis-Associated Chronic Pain: A Preliminary Study

Guillot, Martin; Taylor, Polly M.; Rialland, Pascale; Klinck, Mary P.; Martel-Pelletier, Johanne; Pelletier, Jean-Pierre; Troncy, Eric
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 23/05/2014 EN
Relevância na Pesquisa
45.85%
In cats, osteoarthritis causes significant chronic pain. Chronicity of pain is associated with changes in the central nervous system related to central sensitization, which have to be quantified. Our objectives were 1) to develop a quantitative sensory testing device in cats for applying repetitive mechanical stimuli that would evoke temporal summation; 2) to determine the sensitivity of this test to osteoarthritis-associated pain, and 3) to examine the possible correlation between the quantitative sensory testing and assessment using other pain evaluation methods. We hypothesized that mechanical sub-threshold repetitive stimuli would evoke temporal summation, and that cats with osteoarthritis would show a faster response. A blinded longitudinal study was performed in 4 non-osteoarthritis cats and 10 cats with naturally occurring osteoarthritis. Quantification of chronic osteoarthritis pain-related disability was performed over a two week period using peak vertical force kinetic measurement, motor activity intensity assessment and von Frey anesthesiometer-induced paw withdrawal threshold testing. The cats afflicted with osteoarthritis demonstrated characteristic findings consistent with osteoarthritis-associated chronic pain. After a 14-day acclimation period...

Sphingosine Lysolipids in the CNS: Endogenous Cannabinoid Antagonists or a Parallel Pain Modulatory System?

Selley, Dana E.; Welch, Sandra P.; Sim-Selley, Laura J.
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
45.87%
A significant number of patients experience chronic pain and the intractable side effects of currently prescribed pain medications. Recent evidence indicates important pain modulatory roles for two classes of G-protein-coupled receptors that are activated by endogenous lipid ligands, the endocannabinoid (eCB) and sphingosine-1-phosphate (S1P) receptors, which are widely expressed in both the immune and nervous systems. In the central nervous system (CNS), CB1 cannabinoid and S1P1 receptors are most abundantly expressed and exhibit overlapping anatomical distributions and similar signaling mechanisms. The eCB system has emerged as a potential target for treatment of chronic pain, but comparatively little is known about the roles of S1P in pain regulation. Both eCB and S1P systems modulate pain perception via the central and peripheral nervous systems. In most paradigms studied, the eCB system mainly inhibits pain perception. In contrast, S1P acting peripherally at S1P1 and S1P3 receptors can enhance sensitivity to various pain stimuli or elicit spontaneous pain. However, S1P acting at S1P1 receptors and possibly other targets in the CNS can attenuate sensitivity to various pain stimuli. Interestingly, other endogenous sphingolipid derivatives might play a role in central pain sensitization. Moreover...

Central Sensitization Syndrome and the Initial Evaluation of a Patient with Fibromyalgia: A Review

Fleming, Kevin C.; Volcheck, Mary M.
Fonte: Rambam Health Care Campus Publicador: Rambam Health Care Campus
Tipo: Artigo de Revista Científica
Publicado em 29/04/2015 EN
Relevância na Pesquisa
45.88%
In both primary care and consultative practices, patients presenting with fibromyalgia (FM) often have other medically unexplained somatic symptoms and are ultimately diagnosed as having central sensitization (CS). Central sensitization encompasses many disorders where the central nervous system amplifies sensory input across many organ systems and results in myriad symptoms. A pragmatic approach to evaluate FM and related symptoms, including a focused review of medical records, interviewing techniques, and observations, is offered here, giving valuable tools for identifying and addressing the most relevant symptoms. At the time of the clinical evaluation, early consideration of CS may improve the efficiency of the visit, reduce excessive testing, and help in discerning between typical and atypical cases so as to avoid an inaccurate diagnosis. Discussion of pain and neurophysiology and sensitization often proves helpful.

Antagonism of the chemokine receptors CXCR3 and CXCR4 reduces the pathology of experimental autoimmune encephalomyelitis

Kohler, R.; Comerford, I.; Townley, S.; Haylock-Jacobs, S.; Clark-Lewis, I.; McColl, S.
Fonte: Int Soc Neuropathology Publicador: Int Soc Neuropathology
Tipo: Artigo de Revista Científica
Publicado em //2008 EN
Relevância na Pesquisa
65.78%
Chemokines regulate lymphocyte trafficking under physiologic and pathologic conditions. In this study, we have investigated the role of CXCR3 and CXCR4 in the activation of T lymphocytes and their migration to the central nervous system (CNS) using novel mutant chemokines to antagonize CXCR3 and CXCR4 specifically. A series of truncation mutants of CXCL11, which has the highest affinity for CXCR3, were synthesized, and an antagonist, CXCL11((4-79)), was obtained. CXCL11((4-79)) strongly inhibited the migration of activated mouse T cells in response to all three high-affinity CXCR3 ligands, CXCL9, 10 and 11. CXCL12((P2G2)), while exhibiting minimal agonistic activity, potently inhibited the migration of activated mouse T cells in response to CXCL12. Interfering with the action of CXCR3 and CXCR4 with these synthetic receptor antagonists inhibited experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis and reduced the accumulation of CD4(+) T cells in the CNS. Further investigation demonstrated that CXCL12((P2G2)) inhibited the sensitization phase, whereas CXCL11((4-79)) inhibited the effector phase of the immune response. Our data suggest that simultaneous targeting of CXCR4 and CXCR3 may be of benefit in the treatment of the CNS autoimmune disease.; The definitive version may be found at www.wiley.com

TMD and chronic pain: A current view

Furquim,Bruno D'Aurea; Flamengui,Lívia Maria Sales Pinto; Conti,Paulo César Rodrigues
Fonte: Dental Press International Publicador: Dental Press International
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/02/2015 EN
Relevância na Pesquisa
65.93%
This review aims at presenting a current view on the physiopathologic mechanisms associated with temporomandibular disorders (TMDs). While joint pain is characterized by a well-defined inflammatory process mediated by tumor necrosis factor-α and interleukin, chronic muscle pain presents with enigmatic physiopathologic mechanisms, being considered a functional pain syndrome similar to fibromyalgia, irritable bowel syndrome, interstitial cystitis and chronic fatigue syndrome. Central sensitization is the common factor unifying these conditions, and may be influenced by the autonomic nervous system and genetic polymorphisms. Thus, TMDs symptoms should be understood as a complex response which might get worse or improve depending on an individual's adaptation.