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)

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

Three types of clinical features at the onset are well known to be characteristic of acute hemiplegia syndrome (AHS). Type 1 comprises status epilepticus of hemiconvulsions with fever. Representative diseases of this type are the infectious diseases of the central nervous system, acute encephalopathy and cerebral vascular diseases. Type 2 comprises status epilepticus of hemiconvulsions without fever. Cerebral vascular diseases and epilepsy are the major ones of this type. Type 3 comprises hemiplegia or hemiparesis of sudden onset without fever or convulsions. Most patients with this type had cerebral vascular diseases, about half of which were moyamoya disease in Japan. Recent progress in neuroimaging studies has allowed considerable elucidation of the etiology of AHS. Gadolinium-enhanced MRI showed minimal lesions such as capsular infarction more clearly than plain MRI. Acetazolamide test 99mTc-HMPAO SPECT imaging is one of the useful assisted diagnostic techniques for moyamoya disease, because it reveals the reserve capacity of the collaterals. [123I]IMP SPECT is useful for the diagnosis and follow-up of acute disseminated encephalomyelitis (ADEM), as the images of the lesions coincide well with the MRI ones. 99mTc-HMPAO SPECT in a case with alternating hemiplegia revealed normoperfusion in the ictal periods. Four cases of AHS are reported here.
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PMID:Acute hemiplegia syndrome in childhood. 805 23

We report a case of acute postinfectious encephalopathy in a child following Campylobacter jejuni enteritis. Serial MR scans showed lesions involving predominantly gray matter and the adjacent subcortical white matter--findings different from those in other immune-mediated disorders, such as systemic lupus erythematosus, in which either white or gray matter may be involved, and acute disseminated encephalomyelitis, in which white matter abnormalities predominate with involvement of the subcortical white matter.
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PMID:Postinfectious encephalopathy in a child following Campylobacter jejuni enteritis. 845 26

Several neurological complications associated with Influenza virus infection are known as a febrile convulsion, polyneuritis, meningitis, encephalomyelitis and encephalopathy. Influenza encephalopathy is the most severe complication associated with Influenza. It may be classified into several subtypes according to the clinical symptoms and laboratory data. In this review, Reye's syndrome, acute necrotizing encephalopathy and hemorrhagic shock and encephalopathy syndrome (HSE) are described in detail. The 1995 influenza pandemia in Nagasaki prefecture was markedly neurovirulent and lethal. Twelve cases developed influenza encephalopathy, and the mortality rate between them was 50%. Almost all of them had never be inoculated of influenza vaccine before.
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PMID:[Neurological outcome associated with influenza viral infection]. 910 88

Despite rapid dissemination of Borrelia burgdorferi throughout the body following initial inoculation, the clinical manifestations of this illness tend to involve specific organ systems preferentially. The nervous system, in particular, is frequently affected; involvement usually follows one of several distinct patterns. Most commonly, patients develop a lymphocytic meningitis, radiculoneuritis or cranial neuropathy, occurring singly or in combination. Patients with radicular involvement often have a myelopathic component as well. At the other extreme, rare patients will develop focal inflammation of the central nervous system, an encephalomyelitis, that appears to involve white matter more often than grey. More commonly, patients may develop cognitive and memory impairment-a mild encephalopathy. In some patients this may represent a subtle form of encephalomyelitis, while in others it is probably a "toxic-metabolic" effect of systemic infection. Disease variability among patients probably is the result of multiple factors, including bacterial strain differences in virulence and organotropism, inoculum size, host immunity, and simultaneous co-infection with other tick-borne organisms. Accurate diagnosis remains somewhat problematic. The cerebrospinal fluid is almost always abnormal in the presence of active CNS infection. Intrathecal production of specific antibody can be demonstrated in over 90% of patients with meningitis or frank inflammatory encephalomyelitis; in patients with a milder encephalopathy this is less consistently observed. In most instances, diagnosis relies on a combination of demonstration of a specific immune response, and clinical judgment. In patients in whom the diagnosis is secure, appropriate antimicrobial therapy is highly effective in the vast majority of cases, although if there has been significant structural damage to the CNS, some residua may remain.
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PMID:Neuroborreliosis: central nervous system involvement. 916 55

We report the case of a 62-year-old man affected by anti-Hu-associated paraneoplastic encephalomyelitis. The underlying tumor was a neuroendocrine cancer of the rectum expressing Hu antigen. The neurologic presentation was limited to moderate sensitive neuropathy associated with two complex partial seizures (dreamy state) without any further signs of limbic encephalopathy. A paraneoplastic etiology should be considered in patients with moderate symptomatology. Paraneoplastic encephalomyelitis with anti-Hu antibodies is not always associated with small-cell lung cancer.
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PMID:[Paraneoplastic encephalomyeloneuritis with anti-Hu antibodies and cancer of the rectum]. 929 26

A 4-year-old boy was admitted with disturbed consciousness following a convulsion. He developed bilateral pyramidal tract signs and showed a decerebrate posture. Laboratory findings revealed severe liver dysfunction and disseminated intravascular coagulation. On the eighth day eight in hospital he developed parkinsonism. However, 5 months from onset he had recovered almost completely. Brain CT on admission showed low density areas in the basal ganglia, thalamus, midbrain and pons. A T2-weighted scan in magnetic resonance imaging (MRI) showed almost symmetrical high signal intensities in both basal ganglia (including putamen, caudate nucleus, globus pallidus), external capsule, internal capsule thalamus, midbrain, pons and white matter of the peribasal ganglia; but a T1-weighted scan showed low signal intensities in the same regions during all phases. Therefore hemorrhagic lesions or the presence of thalamic methemoglobin were excluded. It was considered that the pathogenesis may be cytotoxic cellular edema due to cytotoxic agents or acute metabolic factors. Clinical presentation, laboratory findings and radiological findings were most suggestive of acute necrotizing encephalopathy. As differential diagnoses, acute disseminated encephalomyelitis and brainstem encephalitis were considered.
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PMID:Suspected acute encephalopathy with symmetrical abnormal signal areas in the basal ganglia, thalamus, midbrain and pons diagnosed by magnetic resonance imaging. 931 91

Lyme disease is a multisystem infectious disease caused by tick-borne spirochetes of the Borrelia burgdorferi group. The disease occurs primarily in specific areas of North America, Europe and Asia, reflecting the distribution of the hard-shelled Ixodes ticks that are required for disease transmission. Diagnosis of this infection can be somewhat problematic, although in clinically appropriate settings, serologic testing can be highly useful, particularly if Western blots are used to confirm borderline or positive results. The organism has several specific organotropisms-involvement of the heart, joints and nervous system being particularly common. The nervous system can be involved in one or more ways. Early in infection, patients tend to get a lymphocytic meningitis, cranial neuritis (particularly the facial nerves) or a painful radiculitis. Rarely, an encephalomyelitis can occur. In patients with more protracted and indolent involvement, a more disseminated mononeuropathy multiplex may occur, or a mild, non-focal alteration of cognitive function and memory, i.e. an encephalopathy. In patients with central nervous system involvement, the most sensitive diagnostic test is the demonstration of intrathecal production of anti-Borrelia burgdorferi antibody. Culture, polymerase chain reaction and other techniques appear to be less specific. In most instances, the disease is quite responsive to antimicrobial therapy. Oral treatment with doxycycline has been shown to be effective in meningitis. In more serious cases two to four week courses of parenteral ceffriaxone or cefotaxime are effective in the vast majority of patients.
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PMID:Nervous system Lyme disease. 951 77

Any headache in the course of Lyme disease could be an early manifestation of invasion of the CNS by spirochaetes. The most characteristic symptoms of early neuroborreliosis are meningitis with cranial or peripheral neuropathies connected with radiculopathies, less common are encephalitis and myelitis, neuropathies, polyneuropathies, encephalopathies. Encephalomyelitis is the most serious form of neuroborreliosis. From the pathophysiologic point of view all cranial and peripheral neuropathies are forms of mononeuritis multiplex. Encephalopathy is due to neuroimmunomodulators, like lymphokins and or by toxico-metabolic effect could be connected with each form of systemic borreliosis. Certain diagnosis of neuroborreliosis is based on culturing of B. burgdorferi from CSF, detection of specific antispirochaetal antibodies produced in the subarachnoid space, detection of activated lymphocytes B producing specific antibodies, detection in CSF of other antigens of B. burgdorferi or DNA sequences.
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PMID:[Neurologic borreliosis]. 963 83

Japanese encephalitis (JE) is an acute encephalomyelitis which is a primary viral encephalitis accompanying a viral infection. Clinically, the patient who either resides in an endemic region or who has been exposed to the viral vector (mosquito) may have symptoms including high fever, headache, and impaired consciousness. JE involves many portions of the supratentorial and infratentorial compartments including the brain stem, hippocampus, thalamus, basal ganglia, and white matter. Classically MR imaging demonstrates the lesions of JE as hyperintense on T2-weighted images and hypointense on T1-weighted images. Hemorrhagic transformations have also been described in JE lesions, with corresponding expected T1 and T2 changes. Differential considerations based on the MRI appearance are somewhat broad, including but not limited to primary viral encephalitis, acute encephalopathy, limbic encephalitis, and acute disseminated encephalomyelitis. The therapy for JE is primarily conservative and supportive since there is no specific treatment for JE, and the disease has a high fatality rate. The prognosis depends on the extent of involvement at primary presentation, and on the autoimmune mechanisms of this disease.
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PMID:Japanese encephalitis. 970 74


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