Association between ischaemic stroke aetiology and leptomeningeal collateral status: a retrospective cohort study.

INTRODUCTION: There is limited understanding of the pathomechanistic relationship between leptomeningeal collateral formation and ischaemic stroke aetiology. We aimed to assess the association of leptomeningeal collateral status and ischaemic stroke aetiology, using the widely recognised "Trial of Org 10172 in Acute Stroke Treatment" (TOAST) classification categorising strokes into five distinct aetiologies. METHODS: Retrospective study of consecutively admitted adult ischaemic stroke patients at a Swiss stroke centre. Leptomeningeal collateral status was assessed on admission with single-phase CT-angiographies using a validated 4-point score. Patients were categorised into large-artery atherosclerosis (LAA), cardioembolic (CE), small-vessel disease (SVD) and cryptogenic (CG) according to the TOAST classification. We performed ordinal and binary (poor [collaterals filling ≤50% of the occluded territory] vs good [collaterals filling >50% of the occluded territory] collateralisation) logistic regression to evaluate the impact of TOAST aetiology on collateral status. RESULTS: Among 191 patients, LAA patients had better collateral status compared to non-LAA aetiology (LAA: 2 vs CE: 2 vs SVD: 3 vs CG: 2, pLAA vs non-LAA = 0.04). In weighted multivariate logistic regression, LAA and SVD independently predicted better collateral status (binary models [adjusted odds ratio; aOR]: LAA: 3.72 [1.21-11.44] and SVD: 4.19 [1.21-14.52]; ordinal models [adjusted common odds ratio; acOR]: LAA: 2.26 [95% CI: 1.23-4.15] and SVD: 1.94 [1.03-3.66]), while CE predicted worse collateral status (binary models [aOR]: CE: 0.17 [0.07-0.41]; ordinal models [acOR]: CE: 0.24 [0.11-0.51]). CONCLUSION: The aetiology of ischaemic stroke is associated with leptomeningeal collateral status on single-phase CT-angiography, with LAA and SVD predicting better and CE predicting worse collateral status.

Meningeal lymphatic vessel dysfunction driven by CGRP signaling causes migraine-like pain in mice.

Migraines are a type of headache that occur with other neurological symptoms, but the pathophysiology remains unclear. In this issue of the JCI, Nelson-Maney and authors used constitutive and inducible knockouts of the CGRP receptor components, elegantly demonstrating an essential function of CGRP in modulating meningeal lymphatic vessels (MLVs) in migraine. CGRP was shown to induce rearrangement of membrane-bound gap junction proteins in MLVs, resulting in a reduced CSF flux into cervical lymph nodes. The authors also provided evidence of a primary role for CGRP in modulating neuro-immune function. Finally, by showing that blocking CGRP signaling in MLVs attenuated pain behavior associated with acute migraine in rodents, the authors provided a target for pharmacological blockade of CGRP in relation to primary headache disorders.

Inflammatory response of leptomeninges to a single cortical spreading depolarization.

BACKGROUND: Neurogenic meningeal inflammation is regarded as a key driver of migraine headache. Multiple evidence show importance of inflammatory processes in the dura mater for pain generation but contribution of the leptomeninges is less clear. We assessed effects of cortical spreading depolarization (CSD), the pathophysiological mechanism of migraine aura, on expression of inflammatory mediators in the leptomeninges. METHODS: A single CSD event was produced by a focal unilateral microdamage of the cortex in freely behaving rats. Three hours later intact cortical leptomeninges and parenchyma of ipsi-lesional (invaded by CSD) and sham-treated contra-lesional (unaffected by CSD) hemispheres were collected and mRNA levels of genes associated with inflammation (Il1b, Tnf, Ccl2; Cx3cl1, Zc3h12a) and endocannabinoid CB2 receptors (Cnr2) were measured using qPCR. RESULTS: Three hours after a single unilateral CSD, most inflammatory factors changed their expression levels in the leptomeninges, mainly on the side of CSD. The meninges overlying affected cortex increased mRNA expression of all proinflammatory cytokines (Il1b, Tnf, Ccl2) and anti-inflammatory factors Zc3h12a and Cx3cl1. Upregulation of proinflammatory cytokines was found in both meninges and parenchyma while anti-inflammatory markers increased only meningeal expression. CONCLUSION: A single CSD is sufficient to produce pronounced leptomeningeal inflammation that lasts for at least three hours and involves mostly meninges overlying the cortex affected by CSD. The prolonged post-CSD inflammation of the leptomeninges can contribute to mechanisms of headache generation following aura phase of migraine attack.

Factores de riesgo asociados a la meningitis eosinofílica causada por Angiostrongylus cantonensis (Nematoda: Metastrongylidae) en Chone, Ecuador / Risk factors associated to eosinophilic meningitis caused by Angiostrongylus cantonensis (Nematoda: Metastrongylidae) in Chone, Ecuador

Introducción: El parásito Angiostrongylus cantonensis es el principal causante de meningitis eosinofílica. En el 2008 se reportó el primer caso en Ecuador y un estudio reciente en la Ciudad de Chone, Manabí, Ecuador determinó una alta prevalencia del parásito en el caracol africano (Achatina fulica). Objetivo: Identificar los factores de riesgo asociados a la meningitis eosinofílica causada por A. cantonensis en la ciudad de Chone. Métodos: Se entrevistaron a 500 personas residentes en la ciudad de Chone y se revisaron las historias clínicas del Hospital General de Chone. Resultados: Se observó que la población de Chone, está expuesta a los siguientes factores de riesgos: consumo de caracoles crudos (7,40 por ciento), el frecuente contacto de las personas con el caracol africano en la casa (67 por ciento), como en el trabajo (51,20 por ciento), el contacto que tienen los niños con caracoles, al jugar en el jardín (76,80 por ciento) y la incorrecta limpieza de los alimentos (54,40 por ciento). En el entorno de la población, se evidenció la presencia del caracol africano cerca de las casas en el 35,20 por ciento y las ratas, en el 50,80 por ciento. Además, el 34 por ciento de la muestra de estudio presentó sintomatología relacionada con meningitis eosinofílica. Se encontró que existía asociación entre la presencia de vectores cerca de las casas y la cantidad de síntomas manifestados por las personas. Conclusiones: Se evidenció que la población de Chone, manifiesta hábitos que exponen a la gente de esta localidad a un alto riesgo de contagio de meningitis eosinofílica(AU)

Introduction: The parasite Angiostrongylus cantonensis is the main causative agent of eosinophilic meningitis. The first case in Ecuador was reported in 2008, and a recent study conducted in the city of Chone, Manabí, Ecuador, determined a high prevalence of the parasite in the African snail (Achatina fulica). Objective: Identify the risk factors associated to eosinophilic meningitis caused by A. cantonensis in the city of Chone. Methods: Interviews were conducted with 500 residents from the city of Chone and a review was carried out of the medical records at Chone General Hospital. Results: It was found that the population of Chone is exposed to the following risk factors: eating raw snails (7.40 percent), frequent contact between people and African snails both at home (67 percent) and at work (51.20 percent), contact between children and snails while playing in gardens (76.80 percent) and washing food items incorrectly (54.40 percent). In the areas surrounding people's households the African snail was found in 35.20 percent and rats in 50.80 percent . Additionally, 34 percent of the study sample had symptoms of eosinophilic meningitis. An association was found between the presence of vectors near the houses and the number of symptoms occurring in people. Conclusions: It was evident that the population of Chone has habits which expose them to a high risk for eosinophilic meningitis(AU)

Efeitos da lidocaína hiperbárica em concentrações crescentes, administrada no espaço subaracnóideo, sobre a medula e meninges: estudo experimental no cão / Effect of the hyperbaric lidocaína in increasing concentrations, managed in the subaracnóideo space, on the marrow and meninges: experimental study in the dog

Em estudo experimental em ratos, a injeçao de lidocaina subaracnoidea a partir da concentraçao de 7,5 porcento, resultou em mudanças neurofuncionais e histopatologicas. O proposito deste estudo foi investigar, em animais vivos as possiveis alteraçoes clinicas e histologicas desencadeadas por injeçoes de lidocaina hiperbarica nas concentraçoes de 5 porcento, 7,5 porcento e 10 porcento, administradasno espaço subaracnoideo de caes. Quarenta animais foram randomizados em quatro grupos que receberam por via subaracnoidea: G1 glicose a 7,5 porcento e 10 porcento, administradas no espaço subaracnoideo de caes. Quarenta animais foram randomizados em quatro grupos que receberam por via subaracnoidea: G1 glioce a 7,5 porcento, G2 lidocaina hiperbarica a 5 porcento, G3 lidocaina hiperbarica a 7,5porcento e G4 lidocaina hiperbarica a 10 porcento. A punçao subaracnoidea foi realizada no espaço intervetebral L6-L7. O volume da solução injetada foi de 1 ml. Os animais foram sacrificados apos sete dias de observaçao em cativeiro.As porçoes lombar e sacral da medula foram removidas para exame histologico, por microscopia optica. Os caes pertencentes aos grupos G1 e G2, ao apresentaram alteraçoes clinicas e histologicas na medula e meninges. Foi observado tres casos em G3, de necrose em focosno tecido medular mas, necrose abrangendo toda a superficie da medula em somente um dos animais e, a despeito dos achados histologicos, um destes caes permaneceu clinicamente normal. No G4, sete caes apresentaram alteraçoes clinicas e histologicas. As mudanças histologicas encontradas variaram de areas de necrose restritas a algumas regioes da medula a necrose em faixa abrangendo toda a superficie medular. Observamos diminuiçao de força muscular nas patas posteriores em seis animais, sendo que em tres deles houve associação em relaxamento de esfincter anal, e em um dos animais, a diminiçao do tonus esfincteriano foi a unica alteraçao clinica obervada. A neurotoxicidade da lidocaina hiperbarica espinhal em concentraçoes supra-clinicas determinou alteraçoes histopatologicas, restritas ao tecido nervoso da medula espinhal. A extensão e gravidade das lesoes foram intimamente relacionadas com a concentração da lidocaina. Lesoes brandas causadas por concentraçoes mais baixas de lidocaina podem nao manifestar alteraçoes clinicas.

C-Reactive protein: re-evaluation of a diagnostic laboratory test

C-reactive protein has been a measure of acute phase reactions to inflammatory for 40 years. Recently improved quantitative assays in serum and cerebrospinal fluid (CSF) have allowed a re-evaluation of its potential as a diagnostic laboratory test. The main advances in the newer methods have been that they can provide rapid (hours) information on the hepatocyte synthesis of this molecule during immune response. We have tested its value in patients with presumed bacterial meningitis. Based on our experience, newer standardized, quantitative assessments of C-reactive protein can be very useful in distinguishing between bacterial and other forms of meningeal irritation during during the first few days of hospitalization. Other investigators have indicated that by serial measurement important information on the resolution or continuation of inflammatory processes can be obtained. We recommend improved standardization of this test, and recalculation of its usefulness as a diagnostic laboratory test.