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)

We report a 9-year-old girl with leukoencephalopathy who demonstrated serologic evidence of a Mycoplasma pneumoniae infection. She had a mild upper respiratory tract illness 10 days prior to admission and developed walking difficulty and somnolence. The neurologic symptoms progressed to semicoma and spastic paraplegia over a few days but began to improve on the fourth day. Cranial computed tomography on the eleventh day revealed an area of diffuse low density in the white matter. Cerebrospinal fluid examination was normal. The patient recovered with minimal motor deficits. Cranial computed tomography was normal. She was diagnosed as having leukoencephalopathy complicated by a Mycoplasma pneumoniae infection. The pathogenesis of this infection is believed to be an allergic reaction to Mycoplasma pneumonia of the central nervous system as well as an acute disseminated encephalomyelitis.
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PMID:Post-infectious leukoencephalopathy as a complication of Mycoplasma pneumoniae infection. 333 13

Three weeks after a mild and presumably infectious illness, a 21-year-old man developed a CNS disorder characterized by involvement of the cerebellum, cerebrum, and brainstem. It progressed, sometimes stepwise, without remission, over five months to being bedfast with total spastic paraplegia, severe ataxia, and unintelligible dysarthric speech. The CSF showed increased levels of protein, IgG, and myelin basic protein, as well as five oligoclonal bands. Because of failure of the patient's condition to respond to prolonged prednisone therapy, poly ICLC was given intravenously weekly for 20 weeks (median dose, 100 microgram/kg). Improvement, evident after the first dose, progressed to the point of ambulation with some assistance. Even though the relation of the patient's marked recovery to poly ICLC therapy remains unproved, this experience provides reason for considering a possible therapeutic role of the drug in postinfectious demyelinating encephalomyelitis and perhaps in multiple sclerosis.
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PMID:Poly ICLC in the treatment of postinfectious demyelinating encephalomyelitis. 723 70

A case of early-onset acute disseminated encephalomyelitis was presented with her brain imaging. Two weeks after a nonspecific upper respiratory infection, a 14-month-old girl developed spastic paraplegia, difficulty in using left upper extremity and mental deterioration with aphasia. Steroid improved her clinical symptoms. However, 9 weeks later, when steroid was almost withdrawn, relapse with meningeal signs appeared. Reinstitution of steroid was started and 8 weeks later when meningeal signs disappeared, rehabilitation by physical therapist was started. Eighteen months later she recovered into normal intelligence and slight gait difficulty walking with left lower extremity weakness. CT showed extensive symmetric low density lesions in bilateral cerebral white matters and they almost resolved 8 months later. MRI showed extensive symmetric high signal lesions in bilateral cerebral white matters which were demonstrable in the sagittal image. Abnormalities in MRI were much improved 4 months later when she began to speak several words again.
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PMID:[Brain imaging in a case of early-onset acute disseminated encephalomyelitis]. 846 Nov 65

Diagnosis depends on the clinical manifestations, blood or cerebrospinal fluid study and MRI findings. Acute and subacute intraparenchymal spinal cord disorders are due to vascular disorders or myelitis. Spinal cord infarction is associated with dissecting aortic aneurysm, surgical clipping of aortic aneurysms, aortic atherosclerosis or hypotension from any cause. Hematomyelia results from trauma, vascular malformations, vasculitis, or a coagulation disorder. Acute infectious myelopathies result from direct invasion of the spinal cord by bacteria, parasite, or virus. The cause of acute or subacute inflammatory disease include multiple sclerosis, Devic disease, acute disseminated encephalomyelitis, SLE, or sarciodosis. Sarcoidosis sometimes requires differential diagnosis with cord tumor. Chronic intraparenchymal spinal cord disorders are due to syringomyelia, familial spastic paraplegia, HTLV-1 associated myelopathy, adrenomyeloneuropathy, and vascular malformations. HTLV-1 associated myelopathy present with progressive spastic paraplegia with bladder disturbance and has antibodies to HTLV-1 in the cerebrospinal fluid and serum. Diagnosis of adrenomyeloneuropathy is made by demonstration of elevated levels of very long chain fatty acids in plasma. Vascular malformations are important lesions because they present a treatable cause of progressive myelopathy.
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PMID:[Medical approach to intraparenchymal spinal cord disorders]. 1278 77

Leukocyte trafficking to the central nervous system (CNS), regulated in part by chemokines, determines severity of the demyelinating diseases multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). To examine chemokine receptor CX3CR1 in EAE, we studied CX3CR1(GFP/GFP) mice, in which CX3CR1 targeting by insertion of Green Fluorescent Protein (GFP) allowed tracking of CX3CR1+ cells in CX3CR1(+/GFP) animals and cells destined to express CX3CR1 in CX3CR1(GFP/GFP) knockouts. NK cells were markedly reduced in the inflamed CNS of CX3CR1-deficient mice with EAE, whereas recruitment of T cells, NKT cells and monocyte/macrophages to the CNS during EAE did not require CX3CR1. Impaired recruitment of NK cells in CX3CR1(GFP/GFP) mice was associated with increased EAE-related mortality, nonremitting spastic paraplegia and hemorrhagic inflammatory lesions. The absence of CD1d did not affect the severity of EAE in CX3CR1(GFP/GFP) mice, arguing against a role for NKT cells. Accumulation of NK cells in livers of wild-type (WT) and CX3CR1(GFP/GFP) mice with cytomegalovirus hepatitis was equivalent, indicating that CX3CL1 mediated chemoattraction of NK cells was relatively specific for the CNS. These results are the first to define a chemokine that governs NK cell migration to the CNS, and the findings suggest novel therapeutic manipulation of CX3CR1+ NK cells.
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PMID:The neuronal chemokine CX3CL1/fractalkine selectively recruits NK cells that modify experimental autoimmune encephalomyelitis within the central nervous system. 1667 47