scholarly journals Electronic Dura Mater Meddling in the Central Nervous System

2017 ◽  
Vol 74 (4) ◽  
pp. 470 ◽  
Author(s):  
Jocelyne Bloch ◽  
Stéphanie P. Lacour ◽  
Grégoire Courtine
Neurosurgery ◽  
1984 ◽  
Vol 15 (1) ◽  
pp. 104-107 ◽  
Author(s):  
Beyhan Özden ◽  
Orhan Barlas ◽  
Uğur Hacthanefioğlu

Abstract Two cases of primary melanoma of the central nervous system originating from the dura mater and without involvement of the leptomeninges are described. In one case, the tumor was located extradurally with firm attachment to the dura mater and dural melanosis. In the other case, the dura was involved diffusely with multiple discrete masses of 1 to 3 mm in diameter. A literature review revealed five other cases of primary dural melanoma. A discussion of the origin of primary dural melanoma is presented.


1946 ◽  
Vol 92 (388) ◽  
pp. 516-531 ◽  
Author(s):  
C. E. H. Turner

Generalized xanthoma is a cholesterol disturbance of the cells, coincident with a normal lipoid content of the blood serum.The case described involves the skull, dura mater, brain, pleura and gallbladder.


2020 ◽  
Author(s):  
Timothy Casselli ◽  
Ali Divan ◽  
Yvonne Tourand ◽  
Heidi L. Pecoraro ◽  
Catherine A. Brissette

ABSTRACTLyme disease, which is caused by infection with Borrelia burgdorferi and related species, can lead to inflammatory pathologies affecting the joints, heart, and nervous systems including the central nervous system (CNS). Inbred laboratory mice are effective models for characterizing B. burgdorferi infection kinetics and host immune responses in joints and heart tissues; however, similar studies are lacking in the CNS of these animals. Here we characterize the kinetics of B. burgdorferi colonization and associated immune responses in the CNS of infected C3H mice during early and subacute infection. B. burgdorferi colonized the dura mater following needle or tick challenge, and induced expression of inflammatory cytokines and a robust IFN response as well as histopathological changes. A sterile IFN response in the absence of B. burgdorferi or inflammatory cytokines was unique to the brain parenchyma, and could provide insights into the mechanism of inflammatory CNS pathology associated with this important pathogen.


2020 ◽  
Vol 225 (9) ◽  
pp. 2885-2895
Author(s):  
Ruslan Hlushchuk ◽  
David Haberthür ◽  
Petr Soukup ◽  
Sebastien F. Barré ◽  
Oleksiy-Zakhar Khoma ◽  
...  

AbstractAnalysis of the angioarchitecture and quantification of the conduit vessels and microvasculature is of paramount importance for understanding the physiological and pathological processes within the central nervous system (CNS). Most of the available in vivo imaging methods lack penetration depth and/or resolution. Some ex vivo methods may provide better resolution, but are mainly destructive, as they are designed for imaging the CNS tissues after their removal from the skull or vertebral column. The removal procedure inevitably alters the in situ relations of the investigated structures and damages the dura mater and leptomeninges. µAngiofil, a polymer-based contrast agent, permits a qualitatively novel postmortem microangio-computed tomography (microangioCT) approach with excellent resolution and, therefore, visualization of the smallest brain capillaries. The datasets obtained empower a rather straightforward quantitative analysis of the vascular tree, including the microvasculature. The µAngiofil has an excellent filling capacity as well as a radio-opacity higher than the one of bone tissue, which allows imaging the cerebral microvasculature even within the intact skull or vertebral column. This permits in situ visualization and thus investigation of the dura mater and leptomeningeal layers as well as their blood supply in their original geometry. Moreover, the methodology introduced here permits correlative approaches, i.e., microangioCT followed by classical histology, immunohistochemistry and even electron microscopy. The experimental approach presented here makes use of common desktop microCT scanners, rendering it a promising everyday tool for the evaluation of the (micro)vasculature of the central nervous system in preclinical and basic research.


1995 ◽  
Vol 73 (5) ◽  
pp. 558-564 ◽  
Author(s):  
M. Göthert ◽  
E. Schlicker ◽  
M. Garbarg ◽  
J.-C. Schwartz ◽  
J. A. Hey ◽  
...  

As a result of intensive research during several decades, the distribution, function, and pathophysiological role of cardiovascular H1 and H2 receptors are well known, whereas reports on the occurrence and function of H3 receptors in blood vessels and the heart have not become available before the last 7 years (i.e., 4 years after the first description of these receptors in the central nervous system in 1983). The development of selective and potent H3 receptor agonists and antagonists was a prerequisite for convenient investigations of cardiovascular H3 receptors, which like H1 and H2 receptors are G-protein coupled but unlike them have not yet been cloned. Both in blood vessels and the heart, H3 receptors are located on noradrenergic nerve endings and upon stimulation mediate an inhibition of noradrenaline release. Whereas it remains to be clarified under which conditions the vascular H3 receptors may be stimulated by endogenous histamine, those in the heart become activated in the early phases of myocardial ischemia characterized by an increased histamine spillover. The H3 receptors in the central nervous system also appear to be of importance for the control of vascular function. Inhibitory presynaptic H3 receptors occur on trigeminal sensory C fibres supplying blood vessels in the dura mater. Release of neuropeptides from these fibres induces a neurogenic inflammation, which has been suggested to be involved in the pathogenesis of migraine. An interaction, involving presynaptic H3 receptors, between sensory C fibres and mast ceils in close apposition to these fibres plays a role in the control of histamine synthesis in the dura mater. By influencing this regulatory process, H3 receptor agonists may limit the extent of the neurogenic inflammation involved in the pathophysiology of migraine.Key words: histamine receptors, H3 receptors, presynaptic receptors, noradrenaline release, migraine.


2021 ◽  
Vol 17 (2) ◽  
pp. e1009256
Author(s):  
Timothy Casselli ◽  
Ali Divan ◽  
Emilie E. Vomhof-DeKrey ◽  
Yvonne Tourand ◽  
Heidi L. Pecoraro ◽  
...  

Lyme disease, which is caused by infection with Borrelia burgdorferi and related species, can lead to inflammatory pathologies affecting the joints, heart, and nervous systems including the central nervous system (CNS). Inbred laboratory mice have been used to define the kinetics of B. burgdorferi infection and host immune responses in joints and heart, however similar studies are lacking in the CNS of these animals. A tractable animal model for investigating host-Borrelia interactions in the CNS is key to understanding the mechanisms of CNS pathogenesis. Therefore, we characterized the kinetics of B. burgdorferi colonization and associated immune responses in the CNS of mice during early and subacute infection. Using fluorescence-immunohistochemistry, intravital microscopy, bacterial culture, and quantitative PCR, we found B. burgdorferi routinely colonized the dura mater of C3H mice, with peak spirochete burden at day 7 post-infection. Dura mater colonization was observed for several Lyme disease agents including B. burgdorferi, B. garinii, and B. mayonii. RNA-sequencing and quantitative RT-PCR showed that B. burgdorferi infection was associated with increased expression of inflammatory cytokines and a robust interferon (IFN) response in the dura mater. Histopathologic changes including leukocytic infiltrates and vascular changes were also observed in the meninges of infected animals. In contrast to the meninges, we did not detect B. burgdorferi, infiltrating leukocytes, or large-scale changes in cytokine profiles in the cerebral cortex or hippocampus during infection; however, both brain regions demonstrated similar changes in expression of IFN-stimulated genes as observed in peripheral tissues and meninges. Taken together, B. burgdorferi is capable of colonizing the meninges in laboratory mice, and induces localized inflammation similar to peripheral tissues. A sterile IFN response in the absence of B. burgdorferi or inflammatory cytokines is unique to the brain parenchyma, and provides insight into the potential mechanisms of CNS pathology associated with this important pathogen.


1977 ◽  
Vol 46 (3) ◽  
pp. 328-335 ◽  
Author(s):  
Eugene S. Flamm ◽  
Harry B. Demopoulos ◽  
Myron L. Seligman ◽  
John J. Tomasula ◽  
Vincent DeCrescito ◽  
...  

✓ Two models have been used to study the effects of ethanol on injuries of the central nervous system. The spinal cords of cats were injured by delivering a 200 gm-cm impact to the exposed dura mater. A second group of animals received a similar injury to the exposed dura mater overlying the cerebral hemispheres. The animals were divided into two groups, those that received an infusion of ethanol before injury, and control animals that received no ethanol. The parameters of injury used in this model produced small and insignificant lesions in those animals that received no ethanol; however, when the animals were pretreated with ethanol, a considerable increase in the extent of the injury was noted. The mechanisms by which this potentiation is produced are briefly discussed. These include alterations in membrane-bound enzymes and clotting mechanisms, and alteration of cell membranes through abnormal free radical reactions.


Author(s):  
Gladys Harrison

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.


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