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 pathological and immunohistochemical findings of avian encephalomyelitis (AE) were described in various tissues of naturally infected pigeons of a flock from a outbreak in Turkey. Clinically, paresis, paralysis, circling movement and torticollis of the head associated with nervous signs were marked symptoms among the diseased pigeons. At necropsy, small or large white-greyish foci were detected in the pancreas, and erosive-ulcerative foci along with petechial hemorrhages in ingluves. Histopathologically, lesions in central nervous system, particularly in the cerebellum molecular layer, consisted of non-suppurative encephalomyelitis. Lesions in the pancreas revealed non-suppurative pancreatitis along with acinar degeneration and necrosis and/or lymphoid aggregations. Immunohistochemical staining of formalin-fixed, paraffin-embedded tissues was performed using a direct-fluorescein antibody technique with chicken anti-AE virus serum fluorescein isothiocyanate conjugate. Viral antigen was strongly stained in cytoplasm of epithelial cells of the exocrine glands, and neurons of the cerebral hemispheres and midbrain. In addition, viral antigen was also marked in the kidneys and tissues of the digestive system. Consequently, this article is, to our knowledge, the first report of natural AE in pigeons.
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PMID:Avian encephalomyelitis in naturally infected pigeons in Turkey. 1522 70

Erythropoietin (EPO), originally recognized for its central role in erythropoiesis, has been shown to improve neurological outcome after stroke. Here, we investigated the treatment of experimental autoimmune encephalomyelitis (EAE) in mice with EPO. Mice were treated with recombinant human EPO (rhEPO) upon onset of paresis. Neurological functional tests were scored daily by grading of clinical signs (score 0-5). Hematoxylin and eosin (HE) staining of cerebral tissue was performed to detect inflammatory infiltrates. Double staining for Luxol fast blue and Bielshowsky was used to demonstrate myelin and axons, respectively. Immunohistochemistry was performed to measure the expression of bromodeoxyuridine (BrdU, a marker for cell proliferation), NG2 (a marker for oligodendrocyte progenitor cells) and brain-derived neurotrophic factor (BDNF). Treatment with rhEPO significantly improved neurological functional recovery, reduced inflammatory infiltrates and demyelination, and increased oligodendrocyte progenitor cell proliferation and BDNF+ cells compared to the EAE controls. These data indicate that rhEPO treatment improved functional recovery after EAE in mice, possibly, via stimulating oligodendrogenesis, downregulating proinflammatory infiltrates and by elevating BDNF expression.
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PMID:Erythropoietin treatment improves neurological functional recovery in EAE mice. 1571 57

We investigated the treatment of remitting-relapsing experimental autoimmune encephalomyelitis (EAE) in mice with human bone marrow stromal cells (hBMSCs). hBMSCs were injected intravenously into EAE mice upon onset of paresis. Neurological functional tests were scored daily by grading clinical signs (score 0-5). Immunohistochemistry was performed to measure the transplanted hBMSCs, cell proliferation (bromodeoxyuridine, BrdU), oligodendrocyte progenitor cells (NG2), oligodendrocytes (RIP), and brain-derived neurotrophic factor (BDNF). The maximum clinical score and the average clinical scores were significantly decreased in the hBMSC-transplanted mice compared to the phosphate-buffered-saline-treated EAE controls, indicating a significant improvement in function. Demyelination significantly decreased, and BrdU(+) and BDNF(+) cells significantly increased in the hBMSC-treated mice compared to controls. Some BrdU(+) cells were colocalized with NG2(+) and RIP(+) immunostaining. hBMSCs also significantly reduced the numbers of vessels containing inflammatory cell infiltration. These data indicate that hBMSC treatment improved functional recovery after EAE in mice, possibly, via reducing inflammatory infiltrates and demyelination areas, stimulating oligodendrogenesis, and by elevating BDNF expression.
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PMID:Human bone marrow stromal cell treatment improves neurological functional recovery in EAE mice. 1590 21

A pelvic limb paresis of 6 weeks duration in a yearling sheep resulted from protozoan encephalomyelitis involving the spinal cord at the thoracolumbar junction. An elevated lumbosacral cerebrospinal fluid protein concentration but normal cisternal cerebrospinal fluid protein concentration indicated the presence of a thoracolumbar inflammatory lesion resulting in cord compression which obstructed the rostral flow of the cerebrospinal fluid. Under general anaesthesia, myelography at the lumbo-sacral site demonstrated blockage to the rostral flow of contrast medium at T13/L1. At necropsy, there were no gross pathological changes at T13/L1, but histopathology revealed non-tract specific lymphocytic perivascular cuffing, axonal swelling and oedema in the spinal cord, characteristic of a protozoal encephalomyelitis. No parasites were detected in the multiple spinal cord sections examined but immunocytochemistry identified antigens cross-reactive with Sarcocystis spp. antigens in glial cells in these lesions.
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PMID:Protozoan encephalomyelitis causing pelvic limb paresis in a yearling sheep. 1603 13

A 27-year-old woman presented with acute paresis after taking an oral polio vaccine (OPV). Deep tendon reflexes were preserved, needle electromyography showed no neurogenic changes, and there were no lesions on spine magnetic resonance imaging (MRI), suggesting that motor neurons of the spinal cord were not affected. Brain MRI showed abnormal lesions in the tegmentum of the upper pons, left cerebral peduncles, truncus of the corpus callosum, and right parietal lobe. Cerebrospinal fluid revealed mild pleocytosis. The most probable diagnosis was acute disseminated encephalomyelitis associated with OPV.
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PMID:Acute disseminated encephalomyelitis associated with oral polio vaccine. 1710 58

We report a 15 year-old female presenting with behavioral disturbances, headache, left hemiparesis and paresis of the vertical gaze. CAT scan and magnetic resonance showed an involvement of right thalamus, third ventricle and medial temporal lobe suggesting an encephalitis or lymphoma. 201Thalium SPECT suggested a lymphoma. A stereotaxic biopsy showed a subacute demyelinizing lesion, compatible with an acute disseminated encephalomyelitis. The patient was treated with Methylprednisolone with resolution of symptoms. She remains in good condition after one year of follow-up.
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PMID:[Diagnosis of acute disseminated encephalomyelitis using a stereotaxic biopsy: Report of one case]. 1713 Sep 72

Tick-borne borreliosis (Borrelia burgdorferi) is a common and complex disorder affecting the skin, the joints and the nervous system. It progresses through different clinical stages. The clinical spectrum of neuroborreliosis has expanded since the introduction and widespread application of specific serological tests. We have investigated 41 patients with Bannwarth's meningopolyneuritis (MPN) as the classical form of neuroborreliosis, in a prospective (26 patients) and a retrospective (15 patients) study. When questioned, 19/41 patients reported a tick bite and only 15/41, erythema migrans as the characteristic early skin lesion. In 34/41 patients typical MPN characterized by painful radiculoneuritis and/or cranial neuritis, especially facial palsy, were seen. Among these, 3 had a complicated form with a progressive remitting relapsing course or focal central nervous system involvement (hemiparesis, cerebellar syndrome); 2 had mild meningitis and facial nerve palsy bilaterally without radicular pain; and in 5 radicular pain was the only symptom. MPN associated with Lyme arthritis was observed only once. In 2 patients in the retrospective study (no antibiotics in the acute stage) we saw a chronic spinal cord disorder with spastic paresis several years after uncomplicated MPN, accompanied in 1 of them by acrodermatitis chronica atrophicans (ACA), the typical late-onset borrelia-induced dermatosis. In the acute stage of the disease 40/41 patients had a cerebrospinal fluid (CSF) syndrome compatible with MPN (mononuclear pleocytosis, blood-brain barrier dysfunction, elevated IgG and/or oligoclonal bands). IgG antibody titers against borrelia antigen were elevated in all patients in the serum and in 21/30 also in the CSF. In all patients pain was an early and prominent symptom; the first symptoms are usually felt in the region of the tick bite or the erythema, initially as diffuse myalgia, arthralgia or pain in the connective tissue. In the further course the migrating pain becomes more radicular in character, without being limited to defined dermatomic areas or peripheral nerves. The intense, burning pain is characterized by exacerbation during the night. Peripherally and centrally acting analgesics have only minor effects. Often neurological deficits are still absent at this time. Erythema migrans with radicular pain in the region of the dermatological lesion was observed in 2 patients. This is an early manifestation of MPN. After MPN and/or Lyme arthritis a sympathetic reflex dystrophy (SRD) developed in 2 patients. In a further patient SRD was observed right at the beginning of the illness, immediately before MPN. There is a close clinical similarity between SRD and the acute stage of ACA. Therefore, borreliosis can be assumed to produce a painful skin dystrophy like SRD or ACA by direct injury to the sympathetic nerves even in the early clinical stage of the infection. The main conditions to be considered in the differential diagnosis are polymyalgia rheumatica; lumbar disk herniation; inflammatory radiculopathies of other origin (e.g. herpes zoster); painful neuropathies, including the diabetic thoraco-abdominal form; internal disorders of chest and abdomen with referred pain; lymphocytic meningitis of other origin, encephalomyelitis; and sympathetic reflex dystrophy. High-dose penicillin G i.v. is a potent analgesic in all patients with tick-borne neuroborreliosis.
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PMID:[Pain syndromes in tick-borne neuroborreliosis. Clinical aspects and differential diagnosis.]. 1841 56

A 31-year-old woman with Crohn's disease that had been refractory to drug therapies for 7 years had been treated with infliximab for a year. She was admitted to our hospital because of truncal ataxia and bulbar palsy, which presented following aseptic meningitis. Neurological examination revealed abducens paresis on the left, gaze-evoked nystagmus on upward and rightward gaze, right facial muscle weakness, bulbar palsy, weakness in the right upper extremity, limb ataxia predominantly on the left side, diminished sense in the lower extremities predominantly on the right, diffuse hyperreflexia in all extremities. Antibodies to Epstein-Barr virus (EBV) in serum demonstrated a previous infection pattern, and EBV-DNA was detected in peripheral blood and cerebrospinal fluid (CSF) by PCR. CSF analysis indicated pleocytosis, an elevation of IgG index and a marked increase in the level of myelin basic protein. FLAIR MRI images revealed multiple hyperintense lesions in the brainstem, subcortical white matter, and cervical spinal cord. Accordingly, we diagnosed her as having acute disseminated encephalomyelitis (ADEM), associated with reactivated EBV infection. Although gancyclovir, plasma exchange and intravenous high dose immunoglobulins were not effective, repetitive use of methylprednisolone pulse therapy alleviated her symptoms and the abnormal MRI lesions. It is suggested that the reactivated EBV infection caused by infliximab may have contributed to the development of ADEM in this case. Besides the demyelinating event directly induced by anti-TNF-alpha therapy, we should pay attention to the occurrence of reactivated EBV-triggered ADEM during anti-TNF-alpha therapy.
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PMID:[A case of acute disseminated encephalomyelitis associated with Epstein-Barr virus reactivation during infliximab therapy]. 2068 Dec 62

A 51-year-old woman had developed fever and consciousness disturbance at 47 years of age. Brain magnetic resonance imaging (MRI) revealed acute disseminating encephalomyelitis (ADEM)-like lesions without gadolinium enhancement (GDE). One year later, she had an episode of bilateral optic neuritis and cerebellar ataxia. Speech deficit and right hand weakness occurred at the age of 51 years. Neurological examination showed motor aphasia, finger agnosia, right-left disorientation, and right hand paresis. Neuromyelitis optica (NMO)-IgG was seropositive. Cerebrospinal fluid examination showed negative results for myelin basic protein and oligoclonal IgG band. The IgG index was normal. Brain MRI revealed a tumefactive lesion in the left temporo-parietal region and conglomerate ovoid lesions in the pericallosal regions. No GDE was found in the brain lesions. Visual evoked potential test showed bilateral prolongation of P100 latencies. She was treated twice with methylprednisolone pulse therapy followed by oral prednisolone, but the motor aphasia did not respond to steroid treatment. She had no prior history of myelitis and was diagnosed as NMO spectrum disorder (NMOSD). Similar to previous studies of NMO-IgG seropositive extensive brain lesions, this patient with NMOSD indicated no GDE in tumefactive lesions at two episodes of encephalopathy. Compared to multiple sclerosis (MS), a high frequency of non-enhancing tumefactive lesions is reported in patients with NMO or NMOSD. The absence of GDE in tumefactive lesions could help to differentiate between NMO and MS.
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PMID:Repeated non-enhancing tumefactive lesions in a patient with a neuromyelitis optica spectrum disorder. 2153 34

In February and March 2009, approximately 1,500 backyard pigs of variable age became sick, and approximately 700 of them died or were euthanized in the Lower Artibonite Valley and the Lower Plateau of the Republic of Haiti. The main clinical sign was posterior ataxia followed by paresis and/or paralysis on the second or third day of illness. No gross lesions were observed at postmortem examinations. The morbidity and mortality were approximately 60% and 40%, respectively. Diagnostic samples (whole blood, brain, tonsil, lymph nodes, spleen, and lung) were negative for Classical swine fever virus and African swine fever virus. Porcine teschovirus type 1 was detected by reverse transcription polymerase chain reactions in brain samples. Results of virus isolation, electron microscopy of virus particles, histopathological analysis on brain tissues, nucleic acid sequencing, and phylogenetic analysis of the viral isolate supported the diagnosis of teschovirus encephalomyelitis. The outbreak of the disease in Haiti is the first appearance of the severe form of teschovirus encephalomyelitis in the Americas. This disease poses a potential threat to the swine industries in other Caribbean countries, as well as to Central and North American countries.
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PMID:Diagnosis of Porcine teschovirus encephalomyelitis in the Republic of Haiti. 2260 74


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