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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three aspects of the pathophysiology of experimental autoimmune encephalomyelitis (EAE) are discussed: firstly, the possible electrophysiological effects in the CNS of myelin basic protein, which is released during demyelination; secondly, the partial degeneration of monoaminergic and glutamatergic neurons which occurs during an attack of EAE in addition to demyelination; thirdly, the importance of ischemic events, accompanied by free radical release, in EAE. Especially the third aspect could have therapeutic implications. Treatment with radical scavengers, N-methyl-D-aspartate receptor blockers, or calcium blockers (as suggested for ischemia) might prove effective for EAE. Our present aim is to investigate whether these results are also relevant for MS, for which EAE is an animal model.
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PMID:Some pathophysiological aspects of experimental autoimmune encephalomyelitis. 247 88

A number of CT head scans, covering a 2-year period and showing a variety of distinct curvilinear subinsular lucent lesions, were collected and reviewed. Variations in extent of involvement, tendency toward bilateral symmetry, and clinical background allowed the lesions to be grouped into four general patterns, most of which, to our knowledge, have not been specifically described in the radiologic literature. This project was undertaken first to bring to the attention of those involved in interpretation of cranial CT images several patterns of injury they may not heretofore have been aware of and second to attempt to derive a specific etiology for each of the patterns described. Pattern 1, which appears as a distinct curvilinear lesion (sometimes cystic) apparently limited to the lateral aspect of the putamen, is thought to represent the residua of previous lateral striatal hemorrhage. Pattern 2, occurring in a markedly younger age group appears as relatively symmetrical bilateral subinsular lucencies, which in one case completely resolved. A specific etiology for this pattern remains uncertain. Acute demyelination, either secondary to a variant of anoxic leukoencephalopathy or to a limited form of diffuse encephalomyelitis, is postulated. A third pattern, which extends from generalized deep frontal white-matter lucency across the anterior limb of the internal capsule and tapering posteriorly in the subinsular area is thought to be on the basis of chronic ischemia similar to subcortical arteriosclerotic encephalopathy. The fourth pattern, occurring as a broad band of lucency extending from the frontal horn of the lateral ventricle and also tapering posteriorly is due to relatively proximal occlusion of the lateral lenticulostriate arteries.
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PMID:CT of subinsular infarction and ischemia. 310 79

[14C]Deoxyglucose autoradiograms obtained from rats with experimental allergic encephalomyelitis revealed foci of intense glycolytic activity corresponding to inflamed regions. We suggest that well-known sequelae of the inflammatory response, increased capillary permeability leading to hemoconcentration and hemostasis, result in focal hypoxic stimulation of anaerobic glycolysis. This observation calls attention to ischemia as an important determinant of histopathological and clinical etiology of various inflammatory diseases of the central nervous system.
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PMID:Increased glucose utilization associated with inflammatory brain lesions of experimental allergic encephalomyelitis. 660 99

In this study we used nonradioactive in situ hybridization for the cellular localization of vascular cell adhesion molecule-1 (VCAM-1) mRNA in immune-mediated, ischemic and degenerative diseases of the rat nervous system. In the acute phase of experimental autoimmune encephalomyelitis and neuritis VCAM-1 mRNA was expressed not only on the luminal surface of inflamed vessels but also in perivascular cells suggesting a functional role of VCAM-1 in both endothelial adhesion and local restimulation of autoantigen-specific T cells. Accordingly, perivascular T cell accumulation was most pronounced at sites of local VCAM-1 mRNA expression. In addition, VCAM-1 mRNA was detected in the border zone around photochemically induced cerebral infarcts which is the predeliction site of T cell infiltration and expression of immune activation markers during the first week after ischemia. VCAM-1 mRNA was absent from the center of the infarcts as well as axotomized central and peripheral nerves undergoing Wallerian degeneration. These data indicate that VCAM-1-mediated adhesion processes are involved in immune-mediated and ischemic diseases of the nervous system but not in T cell-independent macrophage recruitment during Wallerian degeneration.
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PMID:Vascular cell adhesion molecule-1 mRNA is expressed in immune-mediated and ischemic injury of the rat nervous system. 886 37

Erythropoietin (EPO), recognized for its central role in erythropoiesis, also mediates neuroprotection when the recombinant form (r-Hu-EPO) is directly injected into ischemic rodent brain. We observed abundant expression of the EPO receptor at brain capillaries, which could provide a route for circulating EPO to enter the brain. In confirmation of this hypothesis, systemic administration of r-Hu-EPO before or up to 6 h after focal brain ischemia reduced injury by approximately 50-75%. R-Hu-EPO also ameliorates the extent of concussive brain injury, the immune damage in experimental autoimmune encephalomyelitis, and the toxicity of kainate. Given r-Hu-EPO's excellent safety profile, clinical trials evaluating systemically administered r-Hu-EPO as a general neuroprotective treatment are warranted.
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PMID:Erythropoietin crosses the blood-brain barrier to protect against experimental brain injury. 1098 41

Erythropoietin (EPO) primarily is produced in the kidney and acts as a principal mediator of the physiologic response to hypoxia by increasing red blood cell production. Astrocytes and neurons in the central nervous system (CNS) also are known to produce EPO in response to hypoxia/ischemia. EPO appears to play a neuroprotective role based on preclinical data demonstrating the ability of recombinant human erythropoietin (r-HuEPO) to shield neurons from hypoxic/ischemic stress when administered intracerebraventricularly. In CNS models, systemically administered r-HuEPO has not been intensely investigated because large glycosylated molecules generally were deemed incapable of crossing the blood-brain barrier (BBB). A collaborative research effort identified expression of EPO receptors on human brain capillaries and a specific receptor-mediated transport of r-HuEPO across the BBB after a single intraperitoneal (IP) injection in rodents, with subsequent protection against various types of neuronal damage. For example, administration of r-HuEPO 24 hours before or up to 6 hours after focal ischemic stroke significantly reduced the extent of infarction. r-HuEPO also attenuated concussive brain injury, kainate-induced seizure activity, and autoimmune encephalomyelitis. These preclinical findings suggest that r-HuEPO may have therapeutic potential for stroke, head trauma, and epilepsy; additional studies are needed to confirm and extend these encouraging observations in animal models.
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PMID:Beyond erythropoiesis: novel applications for recombinant human erythropoietin. 1152 26

A patient with exanthem and fever showed progressive disturbance of consciousness and flaccid quadriplegia predominantly in the lower extremities. Antibiotics, aciclovir, high-dose methylprednisolone (1 g/day for 3 consecutive days) and IVIG (400 mg/kg/day for 5 consecutive days) were not effective. Nerve conduction study and SEP in the lower extremities showed peripheral and central conduction block. EEG showed irregular sharp and slow waves predominantly in the left hemisphere. ABR and SEP in the upper extremities were normal. Consecutive studies of cranial and spinal MRIs showed no abnormalities. A diagnosis of acute disseminated encephalomyelitis (ADEM) was made. We started administration of ultra-high-dose methylprednisolone (5.4 mg/kg/h for 47 hours), the dose for acute spinal cord injury based on the randomized controlled trial of The Third National Acute Spinal Cord Injury Study in the USA. After this, she regained consciousness and the quadriplegia improved. The abnormalities in the electrophysiological studies also normalized. It is thought that the neuroprotective mechanism of ultra-high-dose methylprednisolone could be attributed to its inhibition of lipid peroxidation, secondary, ischemia, energy failure and so on. If the usual treatment is not effective for severe encephalomyelitis cases, we can consider the administration of ultra-high-dose methylprednisolone as one of the new treatment options.
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PMID:[A patient of ADEM with central and peripheral conduction block improved with ultra-high-dose methylprednisolone]. 1247 95

Tumor necrosis factor alpha(TNFalpha) is a crucial mediator involved in the communications between immune and nervous systems in physiological conditions, and its relevance is amplified during disease. Considered originally detrimental and a target for therapeutic intervention, recently it has also gained attention for its protective role, especially in central nervous system (CNS) confined diseases. Thus, TNFalpha has become the key molecule illustrating the peculiar and still not completely understood pathways by which inflammatory and immune reactions occur in the brain. Several human pathologies that lack an efficient therapy and that carry enormous social costs rely on these mechanisms. Thus, further research is needed to improve our knowledge and to allow the identification of therapeutic targets or strategies for immune-mediated inflammatory disease of the CNS in which TNFalpha is primarily involved. We describe here how to induce experimental autoimmune encephalomyelitis, cerebral malaria, and brain ischemia in rodents, and some protocols to analyze them. The application of innovative research strategies or original therapeutic approaches to these experimental models may be rewarding in terms of advancement in a field that is crucial for the management of many human patients.
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PMID:TNFalpha in experimental diseases of the CNS. 1506 39

Because oxidative damage has been known to be involved in inflammatory and autoimmune-mediated tissue destruction, modulation of oxygen free radical production represents a new approach to the treatment of inflammatory and autoimmune diseases. Central nervous system tissue is particularly vulnerable to oxidative damage, suggesting that oxidation plays an important role in the pathogenesis of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Caffeic acid phenethyl ester (CAPE), an active component of honeybee propolis, has been determined to have antioxidant, anti-inflammatory, antiviral, and anticancer activities. We have previously reported that CAPE inhibits ischemia-reperfusion injury and oxidative stress in rabbit spinal cord tissue. The present study, therefore, examined effects of CAPE on oxidative tissue damage in EAE in rats. Treatment with CAPE significantly inhibited reactive oxygen species (ROS) production induced by EAE, and ameliorated clinical symptoms in rats. These results suggest that CAPE may exert its anti-inflammatory effect by inhibiting ROS production at the transcriptional level through the suppression of nuclear factor kappaB activation, and by directly inhibiting the catalytic activity of inducible nitric oxide synthase.
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PMID:Protective effects of caffeic acid phenethyl ester against experimental allergic encephalomyelitis-induced oxidative stress in rats. 1522 72

The rapid development of paraparesis or tetraparesis combined with a bilateral sensory deficit that has a clearly defined rostral border and bladder dysfunction are the principal features of acute transverse myelopathy. Acute partial transverse myelopathy is far much more frequent: its symptoms are asymmetric, sometimes unilateral, and sensory deficit may predominate. An urgent MRI is required to exclude acute spinal cord compression. Diagnosis of ischemic acute transverse myelopathy includes the following elements: sudden onset, neurologic symptoms compatible with infarction in the anterior spinal artery area (by far the most frequent location for spinal cord infarction), and presence of a specific cause of spinal cord ischemia. In all other cases where it is difficult to distinguish spinal cord infarction from myelitis, analysis of the cerebrospinal fluid is essential. Most cases of inflammatory acute transverse myelopathy can be linked to a defined cause. Multiple sclerosis is a major cause of partial acute transverse myelopathy. MRI lesions are usually small, located in the lateral or posterior part of the spinal cord. Diagnostic elements include multiple lesions of multifocal demyelination on the cerebral MRI, oligoclonal bands in the cerebrospinal fluid, and the absence of clinical or laboratory abnormalities that suggest systemic disease. Neuromyelitis optica, also known as Devic's disease, has often been considered a variant form of multiple sclerosis. Recent immunologic studies confirm the hypothesis that it is a distinct entity. Infectious transverse acute myelitis is often of viral origin. It may result from direct viral stress but more frequently follows immunologically-mediated indirect stress. This acute parainfectious myelitis, like postvaccinal myelitis, may be considered as a spinal single-focus form of acute disseminated encephalomyelitis (ADEM). It is important to distinguish the latter from an initial episode of multiple sclerosis, because their prognosis and treatment differ.
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PMID:[Acute transverse myelopathy: inflammatory or ischemic?]. 1609 12


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