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)

The mouse hepatitis virus strain JHM was injected intracerebrally into newborn and weanling rats. Three types of diseases were observed: 1. Acute panencephalitis: Almost all suckling rats became moribund within 6 days. Histologically severe panencephalitis with demyelinating foci was noticed; the foci were similar to those found in mice. Virus was easily detectable in the oligodendroglial cells and neurons both by immunofluorescence and electron microscopy. Infectious virus could be isolated. 2. Subacute demyelinating encephalomyelitis (SDE): Three weeks after infection of weanling rats, about 35% of the animals developed paralysis. Neuropathologically, demyelination with a striking predilection for white matter was observed in the brain stem, optic nerve and spinal cord. Virus was detectable by electron microscopy in degenerating oligodendroglial cells only, which corresponded to the results obtained by the immunofluorescent techniques. Infectious virus could be recovered. 3. Chronic progressive paralysis: Inoculated weanling rats without SDE developed 6 to 8 months later a slowly progressing paralysis of the legs. Hydrocephalus and myelomalacia were present. Viral "footprints" could not be detected.
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PMID:Early and late CNS-effects of corona virus infection in rats. 21 26

Recent research has shown that Toxoplasma gondii, the cause of human toxoplasmosis, is a protozoan close to the genus Isospora, whose life cycle involves cats as the definitive host, and other mammals, including man, and birds as intermediate hosts. Cats shed oocysts in their faeces; these are infective to the intermediate hosts when ingested. But the non-felid intermediate hosts can also become infected by eating other intermediate hosts. Probably most human infections occur in this manner and result from eating raw or insufficiently cooked meats. Most people become infected during their life time, but most infections are benign and unnoticed. Occasionally the disease picture may simulate infectious mononucleosis. However, in intrauterine or neonatal infections the disease may be most severe and chorioretinitis, encephalomyelitis, hydrocephalus or microcephaly may result. Diagnosis depends upon demonstrating the parasite in biopsy material or through changing titres in serological tests.
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PMID:Toxoplasmosis. 60 49

A 27 year old woman developed a cerebellar syndrome with serological evidence of recent Mycoplasma pneumoniae infection. The cranial computed tomographic scan showed effacement of the fourth ventricle, enhancement of the basal meninges and hydrocephalus affecting the lateral and third ventricles. Clinical and radiological recovery occurred over 5 weeks. We propose that this was a manifestation of immune-mediated encephalomyelitis induced by the infection rather than direct invasion of the central nervous system.
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PMID:Cerebellar syndrome with hydrocephalus due to Mycoplasma pneumoniae infection. 221 14

The pathogenesis of murine hepatitis virus, strain JHM, was studied in 6- and 12-week-old C57/BL mice. There was 100% mortality in the 6-week-old mice after intracerebral inoculation. The lesions were characterized by necrotizing encephalomyelitis, without demyelination. Intracerebral inoculation of 12-week-old animals, however, resulted in no morbidity or mortality. The 12-week-old animals showed transient virus replication in the brain, spinal cord, and liver, which was cleared by day 14. Histologic examination showed evidence of ongoing demyelination, concomitant remyelination, and hydrocephalus ex vacuo. Although viral antigen was demonstrated by immunofluorescence in the central nervous system of these animals, no infectious virus was recovered, and immunosuppression regimens did not potentiate the disease.
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PMID:Chronic central nervous system demyelination in mice after JHM virus infection. 625 83

Clinical and histological study of 8 cases of Vilyui encephalomyelitis (VEM), characterized by chronic and acute course has shown that all the features of local non-purulent encephalomyelitis with marked dystrophic and atrophic changes of neural tissue were characteristic of VEM. Immunomorphological reaction that manifested as perivascular and membrane lymphoplasmacytic infiltrations was observed in patients with a more acute VEM course or with exacerbation of chronic VEM. Hydrocephalus is considered as a serious aggravating factor that favours atrophic nervous changes during protracted and chronic VEM course.
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PMID:[Clinical picture and histopathology of Viliuisk encephalomyelitis]. 685 78

The theory of a signal averaging system for noninvasive electro-diagnosis and the measurements of auditory, somatosensory and visual evoked responses have been explained. This diagnosis as a powerful new tool has been demonstrated in different patients with cerebellopontine angle tumor, hydrocephalus, brain stem vascular disease, encephalomyelitis and for determining the hearing threshold in infants.
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PMID:[The auditory, somatosensory and visual evoked potentials in the oto-neurologic diagnosis (author's transl)]. 697 77

Akabane virus, an arthropod-borne Bunyavirus, is the major cause of epizootics of congenital malformations in ruminants in Australia, Japan, Korea, and Israel, and is suspected to be a cause of sporadic outbreaks elsewhere. Blood-sucking insects, such as biting midges, transmit the virus horizontally to vertebrates. Climatic factors influence the seasonal activity and geographic range of the vector population and, therefore, occurrence of related disease. Inoculated ruminants seroconvert rapidly after a short subclinical viremia. Infection is of consequence only if ruminants are pregnant and not protected by adequate specific neutralizing antibodies. In naive pregnant animals, virus may spread hematogenously to replicate and persist in trophoblastic cells of placental cotyledons and subsequently invade the fetus. A distinct tropism for immature rapidly dividing cells of the fetal central nervous system and skeletal muscle results in direct virus-induced necrotizing encephalomyelitis and polymyositis. If fetuses survive, such injury may manifest as arthrogryposis, hydranencephaly, porencephaly, microencephaly, hydrocephalus, or encephalomyelitis at term. The earlier in gestation that fetal infection occurs, the more severe the lesions, reflecting the large population of vulnerable cells and lack of fetal immunocompetency at earlier stages of pregnancy. Injury during the period of critical cell migration and differentiation in organogenesis may substantially disrupt structural development in target organs. Late gestational infections cause nonsuppurative inflammation in the brain and spinal cord, premature birth, or fetal death with stillbirth or abortion. Affected neonates are nonviable. Control is by vaccination but is not always justified economically. Akabane viral infections must be differentiated from infections with other teratogenic viruses (including related Bunyaviruses), inherited conditions, and maternal intoxications. Diagnosis is made by serology and viral isolation.
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PMID:Akabane virus. 772 35

The etiology of hydrocephalus is never established in the majority of clinical cases, while various agents, nutritional deficiencies, and genetic factors have been shown to play a role. Viral infection has been recognized as one of the causative factors in the development of hydrocephalus. The wild-type DA strain of Theiler's murine encephalomyelitis virus (TMEV), which belongs to the family Picornaviridae, causes a chronic demyelinating disease in mice with viral persistence that resembles multiple sclerosis. We found that a DA virus variant, hydrocephalus 101 virus (H101 virus), caused hydrocephalus in mice, a condition previously never described for TMEV. To clarify the relationship between DA virus infection and hydrocephalus, we compared H101 virus and wild-type DA virus infection in mice. Using immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL), we found that during the acute phase of infection, H101 virus caused macrocephaly and meningitis with the presence of apoptosis, while parenchymal involvement was not evident. In contrast, wild-type DA virus caused an acute polioencephalomyelitis with parenchymal infection and apoptosis. During the chronic phase, H101 virus infection caused communicating hydrocephalus without viral persistence. No demyelination and little or no anti-TMEV antibodies were observed in H101 virus-infected mice. Sequence analysis revealed that H101 virus had mutations in the 5'UTR and capsid protein coding region. Characterization of this new hydrocephalus model gives insight into the possible viral involvement in human hydrocephalus cases of obscure etiology.
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PMID:Hydrocephalus in mice infected with a Theiler's murine encephalomyelitis virus variant. 941 79

Extracellular fluid in the central nervous system (CNS) is composed of cerebrospinal fluid (CSF), derived from the choroid plexus, and of interstitial fluid (ISF) in gray and white matter. Investigation of CSF plays a significant role in diagnosis and management of neurological disease and pathologies involving the CSF have important effects on the CNS itself. Hydrocephalus has many causes; clinical effects are due to a mixture of obstruction to CSF flow and damage to periventricular white matter with CSF edema, axonal loss and gliosis. Meningitis and subarachnoid hemorrhage are mainly confined to the subarachnoid space emphasising how this compartment is separated from the CNS by the pia mater and glia limitans; brain damage results from thrombosis of leptomeningeal vessels and infarction of CNS tissue. ISF from white matter appears to drain mainly to CSF, but ISF from gray matter drains along periarterial pathways in CNS and meninges, to lymph nodes in experimental animals, and probably in humans. Beta-amyloid in Alzheimer disease and prion proteins accumulate in the extracellular spaces of gray matter and in periarterial ISF drainage pathways as cerebral amyloid angiopathy, emphasising the role of periarterial drainage for the elimination of high molecular weight substances from the brain, possibly to regional lymph nodes. Lymphatic drainage of ISF drainage plays a major role in B- and T-lymphocyte mediated immune reactions in the CNS in animals. By analogy with experimental autoimmune encephalomyelitis, lymphatic drainage of brain antigens in ISF from the human CNS may play a key role in the pathogenesis of Multiple Sclerosis.
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PMID:Pathology of cerebrospinal fluid and interstitial fluid of the CNS: significance for Alzheimer disease, prion disorders and multiple sclerosis. 978 39

Posterior fossa cysts have been reclassified, migrational defects have been matched with histology, and new abnormalities have been described in neurofibromatosis, tuberous sclerosis and ceroid lipofuscinosis. Normal myelination, progressive hydrocephalus, infantile neoplasms, cryptic angiomas and irreversible anoxic brain damage are reviewed. The distribution of grey matter changes in subacute necrotizing encephalomyelitis is discussed and the superiority of magnetic resonance imaging in partial epilepsy and neurological acquired immune deficiency syndrome is confirmed.
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PMID:Neuroradiology. 1014


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