A rare case of migrainous left bell抯 palsy after migrainous right external ophthalmoplegia - A case report

Migraine increased the risk of Bell palsy in the total population. Among migraine patients, between ?30 and <60 years old are at an increased risk of Bell palsy. A migraine is a primary headache characterized by recurrent headache attacks triggered by various factors. As much as 10% of the global population is thought to experience migraine headaches. It was earlier considered that migraine headaches were triggered by the dilation of cerebral vessels, and the recent evidence supports that migraine attacks can also occur in the absence of vasodilation. According to the researchers, the direct neural effects from the trigeminal nerve to the facial nerve could contribute to the risk of facial palsy among patients with migraine. An alteration of the trigeminovascular function has been suggested to trigger migraines. The neurogenic inflammation of the facial nerve trunk caused by its proximity to the dilated posterior auricular/ stylomastoid/ occipital and superficial temporal arteries during a migraine attack leads to a temporary lower motor neuron type of paresis of the muscles supplied by the facial nerve. We herewith report a rare case of migrainous left Bell抯 palsy after migrainous right external ophthalmoplegia, treated with Sumatriptan.

Modified Sanpiantang Treats Nitroglycerin-induced Migraine in Rats via p38 MAPK/iNOS Signaling Pathway / 中国实验方剂学杂志

ObjectiveTo decipher the mechanism of modified Sanpiantang in the treatment of nitroglycerin-induced migraine in rats. MethodSeventy-two Wistar rats were randomized into the control， model （nitroglycerin， 10 mg·kg-1）， positive control （rizatriptan， 0.89 mg·kg-1）， and high- （12.96 g·kg-1）， medium- （6.48 g·kg-1）， and low-dose （3.24 g·kg-1） modified Sanpiantang groups. The rat model of migraine was established by intraperitoneal injection of 10 mg·kg-1 nitroglycerin. The behavioral test was carried out to measure the mechanical pain thresholds （MPT） of the periorbital region and hindpaw after successful modeling. The serum levels of nitric oxide （NO）， tumor necrosis factor-α （TNF-α）， interferon-γ （IFN-γ）， and interleukin-1β （IL-1β） in rats were determined by enzyme-linked immunosorbent assay （ELISA）. Immunohistochemistry （IHC） was employed to determine the expression of inducible nitric oxide synthase （iNOS） in the trigeminal nucleus caudalis （TNC）. Western blot was employed to determine the protein levels of iNOS and phospho-p38 mitogen-activated protein kinase （p-p38 MAPK） in the TNC. Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR） was performed to measure the mRNA levels of iNOS， p38 MAPK， and IL-1β in the TNC. ResultCompared with the control group， the model group showed decreased MPT （P<0.01）， elevated serum levels of NO， TNF-α， IFN-γ， and IL-1β （P<0.01）， and up-regulated expression levels of p38 MAPK， iNOS， and IL-1β in the TNC （P<0.05， P<0.01）. Compared with the model group， modified Sanpiantang increased the MPT （P<0.05）， and the medium-dose group showed the most significant effect （P<0.01）. In addition， modified Sanpiantang down-regulated the mRNA levels of iNOS， p38 MAPK， and IL-1β and the protein levels of p-p38 MAPK and iNOS in the TNC of migraine rats （P<0.05， P<0.01） and lowered the serum levels of NO， TNF-α， IFN-γ， and IL-1β （P<0.05， P<0.01）. ConclusionModified Sanpiantang may treat migraine by down-regulating the expression of pro-inflammatory factors such as NO， TNF-α， IFN-γ， and IL-1β in the p38 MAPK/iNOS signaling pathway to reduce the neurogenic inflammation.

Advances in corneal nerve regulation of ocular surface microenvironment / 国际眼科杂志(Guoji Yanke Zazhi)

The cornea is a transparent outer layer of the anterior eye segment, innervated by a high density of neural tissue. In the process of corneal innervation, trigeminal ganglion originated corneal nerves traverse different types of corneal cell in the epithelial and stromal layers. Corneal stromal cells, epithelial cells, immune cells, and other cells interact closely to maintain corneal microenvironmental homeostasis. In addition, corneal nerves is associated with the occurrence and development of many ocular surface diseases. Corneal nerves release various active peptides that regulate corneal sensation, maintain epithelial integrity and proliferation, improve wound healing, and manage local inflammation and immune response. This article reviews the advances in the corneal nerve regulation of the ocular surface microenvironment, providing some new ideas for the further study and treatment of corneal nerve-associated diseases.

Glia function in the endocanabinoid system: narrative review / Função da glia no sistema endocanabinoide: revisão narrativa

ABSTRACT BACKGROUND AND OBJECTIVES: Evidence has highlighted a role of glial cell activation, and their interaction with different neural systems, especially the endocannabinoid system, in the mechanisms involved in the chronicity and maintenance of pain. The aim of this review is to bring an update on published data that demonstrate the interaction between glial cells and the endocannabinoid system in the pathophysiology of chronic pain and its treatment. CONTENTS: A narrative review was performed based on a research in the Medline database, using the Keywords "endocannabinoid", "glial cells", "microglial", "astrocytes", "neuroinflammation". CONCLUSION: Deepening the knowledge about the function of glial cells in the endocannabinoid system will open the possibility of acting on the pathophysiological origin of the pain chronification process, attenuating the mechanisms involved in central sensitization.

RESUMO JUSTIFICATIVA E OBJETIVOS: A evidência científica tem ressaltado um papel da ativação das células da glia e de sua interação com diversos sistemas neurais, com destaque para o sistema endocanabinoide e mecanismos envolvidos na cronificação e manutenção da dor. O objetivo deste estudo foi atualizar os dados publicados que mostrem a interação entre as células da glia com o sistema endocanabinoide na fisiopatologia da dor crônica e seu tratamento. CONTEÚDO: Foi realizada uma revisão narrativa baseada em pesquisa na base de dados Medline, com uso dos unitermos "endocannabinoid", "glial cells", "microglial", "astrocytes", "neuroinflammation". CONCLUSÃO: O aprofundamento do conhecimento acerca da função das células da glia no sistema endocanabinoide abrirá a possibilidade de atuação sobre a origem fisiopatológica do processo de cronificação de dor, atenuando os mecanismos envolvidos na sensibilização central.

Mechanism of neurogenic inflammation and botulinum toxin treatment in rosacea / 中华皮肤科杂志

Localized neurovascular dysregulation is an important factor for the occurrence of rosacea, and it has been confirmed that neurogenic inflammation is a key step in neurovascular dysregulation. Intradermal injection of botulinum toxin can relieve facial flushing and burning sensations, which may be attributed to the inhibition of neuropeptide release from nerve endings and degranulation of mast cells. This review summarizes the research progress in neurogenic inflammation in the pathogenesis of rosacea and botulinum toxin in the treatment of rosacea, aiming to provide a basis for nerve-related basic research and clinical treatment of rosacea.

Research progress on the role of neuropeptides in the pathogenesis of dry eye / 国际眼科杂志(Guoji Yanke Zazhi)

Dry eye(DE)is a multi-factorial ocular surface disease. The mechanisms underlying the pathogenesis of DE is still unclear. Inflammation and immune response are considered to be one of the core mechanisms among the pathogenesis of DE. Neuropeptides are small molecular peptides generated after the sensory nerve endings damaged or stimulated. They play an important role in triggering and regulating inflammatory response. Thus, they are important mediums between the nervous system and immune system. Recent studies have revealed that neuropeptides secreted by ocular surface nerves are considered to be an important factor involved in the pathogenesis of DE. Therefore, this paper summarized the research progress on the roles of neuropeptides underlying the mechanisms of the pathogenesis of DE, analyzed the latest points of view and research hot spots, so as to provide references for the prevention and treatment of DE.

Implications of Transient Receptor Potential Cation Channels in Migraine Pathophysiology / 神经科学通报·英文版

Migraine is a common and debilitating headache disorder. Although its pathogenesis remains elusive, abnormal trigeminal and central nervous system activity is likely to play an important role. Transient receptor potential (TRP) channels, which transduce noxious stimuli into pain signals, are expressed in trigeminal ganglion neurons and brain regions closely associated with the pathophysiology of migraine. In the trigeminal ganglion, TRP channels co-localize with calcitonin gene-related peptide, a neuropeptide crucially implicated in migraine pathophysiology. Many preclinical and clinical data support the roles of TRP channels in migraine. In particular, activation of TRP cation channel V1 has been shown to regulate calcitonin gene-related peptide release from trigeminal nerves. Intriguingly, several effective anti-migraine therapies, including botulinum neurotoxin type A, affect the functions of TRP cation channels. Here, we discuss currently available data regarding the roles of major TRP cation channels in the pathophysiology of migraine and the therapeutic applicability thereof.

Abnormalities in Inflammatory Cytokines Confer Susceptible to Chronic Neuropathic Pain-related Anhedonia in a Rat Model of Spared Nerve Injury

OBJECTIVE: Patients with chronic neuropathic pain (CNP) have a higher incidence to develop depression. However, its pathogenesis has not yet been fully elucidated. Here we aimed to investigate the role of inflammatory cytokines in CNP-related anhedonia, which is a core symptom of depression, and to explore the effects of ketamine and parecoxib on pain and anhedonia. METHODS: A rat model of spared nerve injury (SNI) was constructed to mimic CNP. Hierarchical cluster analysis of sucrose preference test (SPT) was applied to classify the SNI rats into anhedonia susceptible and unsusceptible. Inflammatory cytokines in medial prefrontal cortex (mPFC) of brain, serum and L2–5 spinal cord were measured. Moreover, effects of ketamine or parecoxib on mechanical withdrawal test (MWT) and SPT in anhedonia susceptible rats were detected. RESULTS: Tumor necrosis factor (TNF)-α was increased in mPFC, serum and and spinal cord of anhedonia susceptible rats. Furthermore, anhedonia susceptible and unsusceptible rats both increased the interleukin (IL)-1β level in mPFC, serum and spinal cord. IL-6 was altered in serum and spinal cord, but not in mPFC. IL-10 was significantly altered in mPFC and serum, but not in spinal cord. Additionally, ketamine treatment significantly attenuated the decreased results of MWT and SPT in anhedonia susceptible rats, and that parecoxib significantly improved the MWT score, but failed to alter the result of SPT. CONCLUSION: These findings suggest that abnormalities in inflammatory cytokines confer susceptible to anhedonia in a rat model of SNI. Ketamine, a fast-acting antidepressant, has pharmacological benefits to alleviate pain and anhedonia symptoms.

The sensitization phenomenon of acupoint and biological significances / 中国针灸

In the pathological conditions, the human body induces somatic sensory exchanges and takes neurogenic inflammatory reactions according to referred visceral organ. Acupoint possesses both diagnosing and treating functions according to the acupuncture theory. The sensitization of acupoint refers to a pathophysiological dynamic change which is manifested predominately as a neurogenic inflammatory reaction in the specific area(s) of the body surface under pathological conditions. Furthermore, the process of acupoint from "silent" (physiological status) to "active" (pathological status) is generally represented by the dynamic changes of acupoint location, size and physicochemical environment. These responses of acupoint sensitization simultaneously activate self-healing system in the body and eventually induce the curative effects.

Efficacy Observation of Addition and Subtraction Therapy of Xuanshen Ganju Tang Combined with Sanniutang to Post-infection Cough with Lung Injury Caused by Dryness and Heat / 中国实验方剂学杂志

Objective: To observe the clinical efficacy of addition and subtraction therapy of Xuanshen Ganju Tang combined with Sanniutang to post infection cough (PIC) with lung injury caused by dryness and heat, and investigate its effects on allergic inflammation and neurogenic inflammatory mediators.Method: One hundred and eighty eligible patients with PIC were randomly divided into control group (58 cases) and observation group (122 cases) according to the visiting sequence. Patients in control group got compound methoxyphenamine capsules, 2 capsules/time and tid. Patients in observation group got addition and subtraction therapy of Xuanshen Ganju Tang,combined with Sanniutang, 1 dose/day. The treatment course was 7 days in both groups. Symptom scores for cough (day and night), visual analogue scale of coughing (VAS) and scores for lung injury caused by dryness and heat injury were graded. Time to relieve a cough, time to relieve symptoms, time to vanish cough, and cough recurrence were recorded. Life quality was evaluated by cough-specific quality of life questionnaire (CQLQ), and the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-8 and substance P in sputum neurogenic inflammatory mediators (SP), neuropeptide A (NKA) and calcitonin gene related peptide (CGRP) were detected.Result: Ridit analysis showed that the clinical efficacy in observation group was better than that in control group (PPPPα, IL-1β, IL-6, IL-8, SP, NKA and CGRP in observation group were all lower than those in control group (PConclusion: Addition and subtraction therapy of Xuanshen Ganju Tang combined with Sanniutang can control systems of cough, shorten coughing course, reduce recurrence rate, improve patients' life of quality, and can inhibit allergic inflammation and neurogenic inflammatory mediators in the treatment of PIC with symptom of lung injury caused by dryness and heat, with a better clinical efficacy than pure compound methoxyphenamine capsules.

Drug discovery for Alzheimer's disease based on the functional disturbance of microglia / 药学学报

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease of the brain. Due to the uncertain pathogenesis, prevention and treatment of AD is difficult. Clinic symptoms of AD including progressive loss of memory and spatial orientation are rooted in synaptic and neuronal loss. Unsuccessful clinical trials of several candidate drugs based on amyloid hypothesis and tau hypothesis have led to exploration of new approaches. Neuro-inflammation characterized by dysfunction in microglia is believed to be the hallmark of AD and also the initiator of downstream responses in neurodegeneration. Alleviate microglia activation and neuro-inflammation may delay AD development. In this paper, we describe the current literature on interaction between microglia and neuron, and review the progress in AD drug discovery and neuro-inflammatory inhibitors for treatment of AD.

Anti-inflammation Effects of Chanqin Granules on PM2.5-induced Airway Neurogenic Inflammation Mediated by Nerve Growth Factor in Rats / 广州中医药大学学报

Objective To observe the anti-inflammation effects of Chanqin granules on airway neurogenic inflammation induced by fine particulate matter (PM2.5)and mediated by nerve growth factor (NGF)and to explore the therapeutic mechanism. Methods Forty SD rats were randomly divided into 5 groups,namely saline control group, PM2.5 exposure group, anti-NGF group, Chanqin granules group and Huifeining group (Pseudoephedrine Hydrochloride,Chlorpheniramine Maleate and Dextromethorphan Hydrobromide Solution),8 rats in each group. PM2.5 exposure rat model was established by intratracheal drop infusion of PM2.5 suspension. The rats in PM2.5 exposure group were given gastric gavage of normal saline after PM2.5 exposure , and the anti-NGF group was given gastric gavage of saline after PM2.5 exposure and intraperitoneal injection of anti-NGF agent. Chanqin granules group was given gastric gavage of Chanqin granules (9.36 g·kg-1·d-1)after PM2.5 exposure,Huifeining group was given gastric gavage of Huifeining (8 mL·kg-1·d-1)after PM2.5 exposure,and saline control group was given gastric gavage of normal saline after intratracheal drop infusion of normal saline , the treatment covering 2 weeks. After medication,the contents of substance P (SP),calcitonin gene related peptide(CGRP), neurokinin A(NKA), neurokinin B(NKB), and nerve growth factor(NGF) in rat serum were detected by enzyme-linked immunosorbent assay (ELISA), the expression levels of SP and NGF in lung tissue and dorsal root ganglia were measured by immunohistochemistry , and the protein and mRNA expression levels of NGF in lung tissue and dorsal root ganglia were determined by Western blotting method and reverse transcription quantitative real-time polymerase chain reaction(RT-qPCR),respectively. Results Compared with the saline control group, the levels of SP, NKA, NKB, NGF and CGRP in rat serum, immunohistochemical mean optical density of NGF in lung tissue and SP and NGF in dorsal root ganglia, the protein and mRNA expression levels of NGF in lung tissue and the protein expression level of NGF in dorsal root ganglia of PM2.5 exposure group were all increased(P < 0.05). Compared with PM2.5 exposure group,the above indexes in anti-NGF group, Chanqin granules group, and Huifeining group were decreased (P < 0.05), and there being no differences between the 3 groups (P > 0.05). Conclusion Chanqin granules have certain effects on relieving the neurogenic inflammation in rat airway induced by PM2.5 through inhibiting the expression of NGF.

Does dexamethasone act in neuropeptides SP and CGRP in neurogenic inflammation of the skin? An experimental study

PURPOSE: To investigate the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) after subcutaneous injection of dexamethasone prior to skin incision in rats.METHODS:Twenty seven Wistar-EPM-1 rats were randomly divided into three groups. The sham group (SG) of rats was injected with 0.9 % saline. The second group (Dexa) was injected with 1.0 mg/kg dexamethasone, and the third group (Dexa+) was injected with 10.0 mg/kg dexamethasone. In all groups, the three subcutaneous injections were performed 30 minutes prior to the surgical skin incision and tissue collection. SP and CGRP (15 kDa pro-CGRP and 5 kDa CGRP) were quantified by Western Blotting.RESULTS: No statistically significant differences (p>0.05) were found in pro-CGRP, CGRP and SP values in all three groups.CONCLUSION:The anti-inflammatory effect of dexamethasone did not occur when the substance P and calcitonin gene-related peptide levels were altered during the neurogenic inflammation process of skin wound healing in rats.

Fisiopatología de la migraña: Teoría vascular, ¿Cierta o no? / Pathophysiology of migraine: vascular theory, true or not?

La migraña es una enfermedad de alta prevalencia, incapacitante y en algunas ocasiones de difícil manejo. Desde hace décadas se han planteado múltiples teorías para explicar su curso, su componente genético y la asociación a distintos factores de riesgo. Actualmente se desconoce una fisiopatología única y exacta que implique los eventos, y se ha encontrado fuerte evidencia que muestra que la teoría más antigua y con mayor sustento, a saber la teoría vascular, es en realidad incorrecta, pues no explica la totalidad de los eventos. Sin embargo, se han probado distintos mecanismos que, en conjunto, permiten comprender las alteraciones presentes. Entre estas se cuentan cambios estructurales, implicación de neuropéptidos, sensibilización, e inflamación neurogénica.

Migraine is a highly prevalent disease; it is disabling, and sometimes difficult to manage. For decades, many theories have been proposed to explain its course, its association with a genetic component and with different risk factors. There is currently no single and exact pathophysiology that accounts for all events, and strong evidence has been showing that the oldest theory believed to be mostly true, i.e. the vascular theory, is actually incorrect, because it does not explain the totality of the events. However, various mechanisms have been proven to exist, which together, provide insight into alterations, such as structural changes involving neuropeptides, sensitization, and neurogenic inflammation.

Effects of subcutaneous carbon dioxide on calcitonin gene related peptide and substance P secretion in rat skin

To investigate the subcutaneous injection of carbon dioxide (CO2) on neuropeptides Calcitonin Gene-Related Peptide (CGRP) and Substance P (SP) secretion in rat skin. Fifty-six Wistar-EPM rats were distributed in two groups: one for CGRP analysis, the other for SP analysis. Each group was subdivided into four subgroups: control (Cont), control with needle (ContNd), CO2 injection (CO2Inj) and atmospheric air injection (AirInj) - with seven animals each. Sample analyses of partial skin were conducted by Western Blotting (WB). RESULTS: In SP group, there was a decrease in the amount of neuropeptides in subgroups CO2Inj and AirInj. Similarly, in CGRP group, there was a decrease in the amount of pro-CGRP neuropeptides (15 kDa) in subgroups CO2Inj and AirInj; Nevertheless, there was no decrease in the amount of CGRP (5 kDa) in any subgroups. Subcutaneous injection of CO2 and atmospheric air decreased the amount of Substance P and pro-Calcitonin Gene-Related Peptide (15 kDa) neuropeptides in rat skin.

The change and diagnostic value of airway neurogenic inflammatory mediators in post infection cough / 中国小儿急救医学

Objective To observe the change of neuropeptide of the infant patients with post infection cough (PIC) and explore the possible pathogenesis and diagnostic value.Methods Fifty-two cases with PIC in our hospital were selected as PIC group,while thirty infant patients with bronchopneumonia as pneumonia group.Phlegm cells classification and substance P(S P),neurokinin(NKA),neurokinin (NKB),calcitonin gene-related peptide (CGRP) concentration of the patients in both groups were compared.Results Phlegm cells classification of the two groups showed that,compared with the PIC group,the neutrophils,macrophages,and lymphocytes of the infant patients in the pneumonia group were obviously higher (P ＜ 0.05).After anti-infection treatment,the neutrophils,macrophages and lymphocytes of the infant patients in the pneumonia group were obviously lower(P ＜ 0.01).The phlegm cells classification of the PIC group had not changed significantly before and after treatment (P ＞ 0.05).After treatment,the phlegm cells classification of both groups had no significant difference (P ＞ 0.05).During the progress of treatment,there was no evident change for the eosinophils (P ＞ 0.05).Neuropeptide of the two groups showed that,before treatment,the SP and CGRP of the patients in the PIC group were (538.4 ±432.2) ng/L,(123.6 ±70.2) ng/L,and that in the pneumonia group were (613.2 ± 345) ng/L,(156.2 ± 82.6) ng/L.There was no significant difference (P ＞ 0.05).After treatment,the SP and CGRP of the PIC group were (552.8 ± 421.7) ng/L,(133.5 ± 81.3) ng/L,and there was no significant difference (P ＞0.05).While the SP and CGRP of the patients in the pneumonia group were (156.2 ± 131.2) ng/L,(741.2 ± 35.4) ng/L,they were obviously lower (P ＜ 0.01).There was statistical difference compared with the PIC group after treatment (P ＜ 0.01).The NKA and NKB had not changed significantly before and after treatment.Conclusion Airway neurogenic inflammation mediated SP and CGRP plays a key role in the acute and chronic infections.The increase of SP and CGRP is closely related to the morbidity of PIC.So SP and CGRP is a reference index for early detection of PIC.

Vital tooth with periapical lesion: spontaneous healing after conservative treatment

It is often presumed that apical periodontitis follows total pulp necrosis, and consequently root canal treatment is commonly performed. Periapical lesion development is usually caused by bacteria and its byproduct which irritate pulp, develop pulpitis, and result in necrosis through an irreversible process. Afterwards, apical periodontitis occurs. This phenomenon is observed as an apical radiolucency in radiographic view. However, this unusual case presents a spontaneous healing of periapical lesion, which has developed without pulp necrosis in a vital tooth, through conservative treatment.

Changes in peripheral innervation and nociception in reticular type and erosive type of oral lichen planus.

Background: Oral lichen planus (OLP) is a chronic inflammatory lesion in oral mucosa. Reticular (OLP-R) and erosive (OLP-E) types of OLP are the common forms that have been found in dental clinics. The aim of this investigation is to determine the correlation between neurogenic inflammation and nociception associated with OLP-R and OLP-E. Materials and Methods: The oral mucosal lesions from six patients with OLP-E, four with OLP-R and three with noninflamed oral mucosa, which represent normal mucosa, were identified by morphometric analysis of nerve fibers containing immunoreactive protein gene product (PGP) 9.5. The level of inflammation was measured with hematoxylin and eosin staining and the level of nociception was analyzed with visual analog scale measurement. Results: We found that 1) an increase in peripheral innervation was related to the size of the area of inflammatory cell infiltration from both OLP-R and OLP-E; 2) the pattern of PGP 9.5-immunoreactivity among OLP-R and OLP-E was not significantly different (P=0.23); and 3) the correlation between nociception and an increase in PGP 9.5-immunoreactivity was not found in OLP-E and in OLP-R. Conclusions: Our findings suggest that an increase in peripheral innervation may lead to increased inflammation, which is part of the immunopathogenesis of OLP. Differences in nociception between OLP-R and OLP-E arise from the pathogenesis of each lesion, not from the differences in peripheral innervation.

Nerve growth factor induced expression of iNOS and substance P in dorsal root ganglion sensory neuron and interferon regulatory factor-1 / 中南大学学报(医学版)

Objective To investigate the mechanism of airway neurogenic inflammation by studying the expression of inducible nitric oxide synthase (iNOS) and substance P in C7-T5 dorsal root ganglion sensory neuron cells induced by nerve growth factor (NGF) and the role of interferon regulatory factor-1 (IRF-1).Methods The dorsal root ganglia neuron (DRGn) cells were primary cultured,and then stimulated with or without NGF or NGF+interferon (IFN)-γ.Subsequently the DRGn cells were transinfected with or without green fluorescent protein (GFP)-IRF-1-vshRNA,and then stimulated with or without NGF.The expressions of iNOS and substance P were detected by real-time PCR.Results NGF induced the mRNA expression of iNOS and substance P in dorsal root ganglion sensory neuron cells,and IFN-γ increased NGF-induced iNOS mRNA expression.The expressions of iNOS and substance P in sensory neuron cells were decreased significantly at the mRNA level after IRF-1 was blocked down by IRF-1-vshRNA transinfection.Conclusion NGF is involved in the airway neurogenic inflammation by prompting the expression of iNOS and substance P through transcription factor IRF-1 in airway sensory neuron cells.IRF-1 may be a therapeutic target for airway neurogenic inflammation.

Pioderma gangrenoso e controle álgico: relato de caso / Pyoderma gangrenosum and pain control: case report

JUSTIFICATIVA E OBJETIVOS: O pioderma gangrenoso é uma doença crônica, idiopática, inflamatória, destrutiva levando a dor do tipo neuropática com inflamação neurogênica; se apresenta com lesões ulcerosas, hemorragia e infiltrado de neutrófilos, na maioria dos casos, em ambos os membros inferiores distais, de expansão circunferencial e dolorosa. O objetivo deste estudo foi relatar o caso de paciente com apresentação típica da doença, com dor de difícil controle com analgésicos simples, porém com boa resposta analgésica ao uso de metadona e gabapentina.RELATO DO CASO: Paciente do sexo feminino, 49 anos, com feridas ulcerosas crônicas nos membros inferiores bilaterais, com piora progressiva da dor neuropática das úlceras devido ao insucesso dos enxertos de pele. Foi realizada biópsia da ferida, com diagnóstico de pioderma gangrenoso e realizado tratamento para a dor com metadona, morfina e gabapentina, com bom controle álgico. CONCLUSÃO: O tratamento da dor neuropática com a metadona, que além da ação opioide possui ação moduladora inibitória do receptor de N-Metil-D-Aspartato, e a gabapentina diminuindo a inflamação neurogênica e a liberação de neurotransmissores excitatórios, tais como glutamato e substância P; melhorou a dor de origem neuropática.

BACKGROUND AND OBJECTIVES: Pyoderma gangrenosum is a chronic, idiopathic, inflammatory and destructive disease leading to neuropathic pain with neurogenic inflammation; it presents with ulcers, hemorrhage and neutrophils infiltration, most of the cases on both distal lower limbs. It has circumferential and painful expansion. This study aimed at reporting a case of a patient with typical disease presentation, with pain hardly controlled with simple analgesics, however with good analgesic response to methadone and gabapentine.CASE REPORT: Female patient, 49 years old, with chronic ulcerous wounds on both lower limbs, with progressive worsening of ulcers neuropathic pain due to skin graft failure. Wound was biopsied and pyoderma gangrenosum was diagnosed. Pain was treated with methadone, morphine and gabapentin with satisfactory pain control.CONCLUSION: Treating neuropathic pain with methadone, which in addition to its opioid action has inhibitory modulatory action of the N-Methyl-D-Aspartate receptor, and with gabapentin, decreasing neurogenic inflammation and excitatory neurotransmitters release, such as glutamate and substance P, has improved neuropathic pain.