Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immunohistochemistry was used to study herpes simplex virus type 1-induced central nervous system demyelination in the trigeminal root entry zone of mice inoculated with herpes simplex virus type 1 by the corneal route. There was no change in peripheral nervous system myelin as shown by immunostaining for P0 glycoprotein. Double immunoperoxidase staining for herpes simplex virus type 1 antigens and glial fibrillary acidic protein showed that most of the infected cells were astrocytes. Glial fibrillary acidic protein immunostaining was completely lost in the inferior medial portion of the trigeminal root entry zone at 6 days after herpes simplex virus type 1 inoculation, a time when central nervous system myelin was preserved as indicated by immunostaining for myelin basic protein. The pattern of glial fibrillary acidic protein staining did not change and herpes simplex virus type 1 antigens were no longer detected after day 8. There was a progressive loss of myelin basic protein staining within the area unstained by glial fibrillary acidic protein antisera on days 8 to 14. This pattern of astrocyte loss before central nervous system demyelination is strikingly different from the reactive astrocytosis seen in other demyelinating lesions, such as acute experimental allergic encephalomyelitis, progressive multifocal leukoencephalopathy, or acute multiple sclerosis. Herpes simplex virus type 1 infection in mice provides an unusual model of acute central nervous system demyelination preceded by a loss of astrocytes.
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PMID:Early loss of astrocytes in herpes simplex virus-induced central nervous system demyelination. 204 45

The loss of myelin-associated glycoprotein (MAG) and myelin basic protein (MBP) was compared by quantitative immunocytochemistry in demyelinating lesions of measles encephalomyelitis (ME), multiple sclerosis (MS), and progressive multifocal leukoencephalopathy (PML). Serial sections from paraffin-embedded tissue were reacted with antisera for MAG and MBP, and areas of staining loss were compared morphometrically. Lesions in ME showed MAG loss equal to that of MBP, lesions of PML showed MAG loss greater than that of MBP, and MS lesions showed a mixture of patterns. These data demonstrate distinctive patterns of MAG and MBP loss in these three diseases.
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PMID:A quantitation of myelin-associated glycoprotein and myelin basic protein loss in different demyelinating diseases. 241 98

In the brains and spinal cords of 153 adult patients dying with acquired immunodeficiency syndrome (AIDS) at New York and Memorial Hospitals a subacute encephalitis with multinucleated cells was present in 28% of all patients. This encephalitis was characterized by multinucleated cells primarily located in the white matter and associated with myelin pallor and sparse infiltrates of rod cells, macrophages, gemistocytic astrocytes and lymphocytes. The incidence per 12 month period ranged from 0 to 43% and significantly increased between 1983-84 (14%) and 1984-85 (43%). Recent virologic and pathologic studies suggest that this encephalitis may be caused by direct LAV/HTLV-III infection of the central nervous system (CNS). Cytomegalovirus encephalomyelitis and toxoplasmosis were the most common opportunistic infections (26% and 10%, respectively). Progressive multifocal leukoencephalopathy, herpes simplex ventriculitis, varicella-zoster leukoencephalitis and fungal infections were infrequent (less than 3% each). A nonspecific encephalitis with microglial nodules and with mild white matter changes occurred in 17%, vacuolar myelopathy in 29% and CNS lymphoma in 6%. Less than 20% of patients had either normal brains or terminal metabolic encephalopathies. This survey shows that neuropathologic complications of AIDS are frequent. Infections are the most common complication and are caused by probable LAV/HTLV-III infection, or by opportunistic organisms.
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PMID:Neuropathology of acquired immunodeficiency syndrome (AIDS): an autopsy review. 302 14

A 37-year-old homosexual man with the acquired immune deficiency syndrome (AIDS) developed progressive, ultimately fatal, neurological deficits 12 weeks after a course of cutaneous zoster. Premortem radiological procedures and cerebrospinal fluid analyses were nondiagnostic. At postmortem examination, several opportunistic infections associated with AIDS were recognized. Throughout the brain, necrotic and demyelinative lesions were present, suggestive of progressive multifocal leukoencephalopathy. However, light microscopical examination showed numerous Cowdry type A intranuclear inclusions in astrocytes, oligodendrocytes, and neurons near the periphery of the lesions. Herpes zoster encephalomyelitis was diagnosed and confirmed by electron microscopy, peroxidase-antiperoxidase staining, and by Southern blot analysis of DNA extracted from brain tissue. This case provides insight into the pathogenesis of zoster-associated encephalomyelitis and suggests another agent to be considered in the differential diagnosis of encephalopathy in patients with AIDS and other disorders of immunological impairment.
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PMID:Progressive encephalitis three months after resolution of cutaneous zoster in a patient with AIDS. 396 60

Infectious agents have been postulated as causes of multiple sclerosis for over a century. The possible role of a virus or viruses is supported by data that (1) a childhood exposure is involved and "viral" infections may precipitate exacerbations of disease, (2) experimental infections in animals and natural infections in humans can cause diseases with long incubation periods, remitting and relapsing courses, and demyelination, and (3) patients with multiple sclerosis have abnormal immune responses to viruses. The pathogenesis of three human demyelinating diseases of known viral etiology is discussed. In progressive multifocal leukoencephalopathy, a papovavirus selectively infects oligodendrocytes and causes focal areas of demyelination. In postmeasles encephalomyelitis, the virus is lymphotrophic and disrupts immune regulation that can result in an autoimmune perivenular demyelinating illness without evidence of infection of the central nervous system. In human immunodeficiency virus-encephalopathy and myelopathy virus is present in macrophages and microglia and the myelin abnormalities apparently are caused by soluble factors such as viral proteins, cytokines, or neurotoxins. These findings may have implications on how, when, and where to seek viruses in multiple sclerosis.
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PMID:The virology of demyelinating diseases. 801 89

The progress and extent of myelination can be assessed using magnetic resonance imaging (MRI). Myelination is delayed or diminished in several inherited metabolic abnormalities presenting in early life. Only minimal myelination of the CNS occurs in Pelizaeus-Merzbacher disease. Dysmyelination tends to produce fairly symmetrical lesions affecting white matter. In many mitochondrial enzyme and some lysosomal defects, the grey matter is also involved. The appearances and in particular the distribution on MRI and/or CT are characteristic in some conditions and the diagnosis is limited in others. Demyelination due to inflammatory disorders typically causes multifocal white matter lesions, recurrent in multiple sclerosis, monophasic in acute disseminated encephalomyelitis, extending in progressive multifocal leukoencephalopathy and classically involving the pons or corpus callosum in myelinolysis. Hypoxic ischaemic lesions may be metabolically induced and simulate primary demyelinating disorders. Mitochondrial enzyme defects in particular may present with stroke-like appearances. In many of these conditions, diagnosis is biochemical, but imaging has a significant role in suggesting the diagnosis, and documenting progression, response to therapy or complications.
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PMID:Inborn errors and demyelination: MRI and the diagnosis of white matter disease. 841 20

Most of viral encephalitis may demonstrate no specific change on CT and MR images. Brain swelling, edema, abnormal density (CT) and abnormal intensity (MR) can be detected in herpes simplex encephalitis and enterovirus encephalitis (coxsackie, echo, polio). The common finding on CT and MRI in patients with HIV encephalopathy are atrophy, leukomalacia. Progressive multifocal leukoencephalopathy (PML) shows multifocal oval or round white matter T2-hyperintensities on MR images. Subacute sclerosing panencephalitis (SSPE) may present slight changes in the subcortical and periventricular white matter, as well as basal ganglia. Progressive disorder makes widespread T1-low, T2-high intensity area and atrophy. MRI of acute disseminated encephalomyelitis (ADEM) shows multifocal subcortical hyper intense foci on T2-weighted studies. The deep white matter, brainstem, thalamus and cerebellum can be affected. Most of ADEM lesions resolve. Imaging findings of acute lymphocytic meningitis by echovirus and coxsackievirus are usually normal.
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PMID:[Radiological diagnosis of viral encephalitis]. 910 77

Magnetization transfer imaging is used in multiple sclerosis because of its sensitivity to tissue destruction; in particular, to demyelination. This sensitivity was established in animal models and human diseases. Studies in experimental auto-immune encephalomyelitis have shown that the magnetization transfer ratio is slightly decreased in inflammatory lesions of the central nervous system white matter without demyelination but is more decreased in demyelinated lesions according to the level of myelin loss. Toxic demyelination studies and human studies in progressive multifocal leukoencephalopathy have confirmed that pure moderate to severe demyelination can be monitored by this technique. Axon loss can also contribute to the decrease of this ratio. Magnetization transfer is a validated technique to assess tissue destruction in central nervous system white matter diseases.
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PMID:Pathological correlates of magnetization transfer imaging abnormalities in animal models and humans with multiple sclerosis. 1049 5

Myelin basic protein (MBP) is a major component of the myelin sheath of both the central and peripheral nervous systems. A number of neurological diseases in humans are associated with demyelination of the central and/or peripheral nervous systems, including multiple sclerosis and its variants such as acute disseminated encephalomyelitis (AD), acute hemorrhagic leukoencephalopathy, and idiopathic polyneuritis (Guilliame-Barre syndrome), as well as tropical spastic paraparesis (TSP), and progressive multifocal leukoencephalopathy (PML). Multiple sclerosis (MS) is perhaps the most common demyelinating disease and is one of great importance to the clinical neurologist. The underlying cause of the demyelination seen in multiple sclerosis patients is unknown. However, patients frequently have unusually high antibody titers to a number of common viruses, leading to speculation that viral infections may participate in the pathogenesis of MS. On the other hand, studies on maternal and paternal twins have suggested the involvement of genetic factors in the predisposition of an individual toward developing MS. PML, once a rare demyelinating disease of elderly patients with lymphoproliferative disorders, is now a much more common disease affecting patients of all ages due to the increasingly widespread use of immunosuppressive chemotherapy and the prevalence of AIDS. PML is the result of productive infection of oligodendrocytes, the myelin producing cells of the CNS, with the human polyomavirus, JCV. In this article, we have focused our attention on PML, and the role of JCV in disrupting myelin sheaths by affecting myelin basic gene expression, ultimately leading to demyelination.
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PMID:Human polyomavirus JCV and expression of myelin genes. 1087 94

Various infratentorial pathological conditions can mimic multiple sclerosis (MS) both clinically and radiologically. We review the inflammatory, vascular, neoplastic and metabolic conditions which show features similar to those of MS on magnetic resonance imaging (MRI). Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum. Neoplastic diseases, in particular pontine gliomas and lymphomas, can mimic MS. Vascular ischaemic lesions, either due to infarction produced by occlusion of a major posterior circulation artery or due to small vessel vasculopathy, can lead to posterior fossa lesions. The MRI changes of central pontine myelinolysis can also mimic MS. Diffuse axonal injury, radiation and chemotherapy induce lesions that resemble MS, however the clinical history will exclude these possibilities. Finally, we discuss a few conditions which are similar to MS in clinical presentation but have different MRI appearances, such as brainstem cavernomas, posterior fossa tumoural lesions, aneurysms and vascular loops producing neurovascular conflicts. Analysis of the MRI findings with clinical history and laboratory data helps to narrow down the diagnosis of the infratentorial pathology.
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PMID:Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects. 1179 84


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