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PubMed2000

Postinfectious encephalomyelitis: etiologic and diagnostic trends.

Fifty cases of postinfectious encephalomyelitis admitted to our Pediatric Department during the period 1980 to 1997 were consecutively collected and reviewed. There were 28 males and 22 females. The age of onset ranged from 9 months to 14 years. The antecedent infections included measles (6 cases), rubella (5 cases), mumps (4 cases), chicken pox (4 cases), Epstein-Barr virus infection (11 cases), mycoplasma infection (6 cases), and unknown etiology (14 cases). The cessation of measles, rubella, and mumps as causes for encephalomyelitis in our patients corresponds with the introduction of a measles-mumps-rubella nationwide vaccination program in Taiwan commencing in 1992. The main clinical symptoms were fever, headache, and/or vomiting, seizure, and motor weakness. The presenting signs included altered consciousness, meningeal signs, cranial nerve palsy, brainstem signs, involuntary movement, and cerebellar signs. Computed tomography scans were abnormal for 14 (56%) of 25 patients studied, whereas magnetic resonance imaging (MRI) disclosed lesions in 14 (82%) of 17 patients, with abnormal signals in various parts of the cerebral hemisphere, as well as in the basal ganglion, diencephalon, midbrain, brain stem, and cerebellum. Of the three patients with negative MRI findings, an abnormal finding on somatosensory evoked potential was noted for one patient, and a focal decrease in tracer uptake on single photon emission computed tomography (SPECT) was found for the other two patients. This study demonstrates that the causative agents of postinfectious encephalomyelitis in Taiwan have changed from those of traditional exanthematous diseases to nonspecific respiratory infections and suggests that this may also be the case in other parts of the world. MRI remains the imaging method of choice, whereas other neurofunctional studies such as evoked potentials and SPECT are complementary for the diagnosis.

Adolescent↗
PubMed1991

Steroid-dependent postvaricella encephalomyelitis.

Postinfectious encephalomyelitis is an acute demyelinating illness that usually has its onset 3 to 7 days after the onset of a viral exanthem and has a monophasic course over 2 to 4 weeks. Recurrent bouts of postinfectious encephalomyelitis have been described that have resolved spontaneously or with short courses of steroid therapy. We report a patient who developed a chronic, steroid-dependent encephalomyelitis secondary to a varicella infection at 5 months of age.

Adolescent↗
PubMed1995

Brainstem multiple sclerosis in an 11-year-old child presenting as acute disseminated encephalomyelitis.

Multiple sclerosis and acute disseminated encephalomyelitis are demyelinating disorders of the central nervous system that can present initially as an acute focal demyelinating syndrome. We report an 11-year-old girl who initially presented with intractable vomiting and hypertension and later developed a subacute onset of focal neurologic (brainstem) signs. Magnetic resonance imaging (MRI) demonstrated a large solitary demyelinating lesion of the brain stem consistent with acute disseminated encephalomyelitis. Because of the morbidity associated with biopsy and its questionable value in the course of management of this patient, she was treated empirically with aggressive supportive measures and high-dose corticosteriod therapy. She had near full recovery, with only minimal neurologic sequelae. Six months later, she presented with similar focal neurologic signs, and a new lesion was found on MRI. Because of the separation of her two episodes in time and central nervous system location, a diagnosis of multiple sclerosis was made. Herein, we used this patient to illustrate the difficulty in distinguishing acute disseminated encephalomyelitis from multiple sclerosis in patients who present initially with an acute focal demyelinating syndrome.

Brain Stem↗
PubMed2001

Disease progression in chronic relapsing experimental allergic encephalomyelitis is associated with reduced inflammation-driven production of corticosterone.

In this study, we demonstrate that disruption of neuroendocrine signaling is a major factor driving disease progression in myelin oligodendrocyte glycoprotein-induced chronic relapsing experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis. Although the initial episode of chronic relapsing experimental autoimmune encephalomyelitis is associated with a robust hypothalamic-pituitary-adrenocortical axis response, we show that subsequent disease progression is associated with a selective desensitization of hypothalamic-pituitary-adrenocortical responsiveness to inflammatory mediators. Inflammatory activity in the central nervous system during relapse is therefore unable to produce an endogenous immunosuppressive corticosterone response, and disease progresses into an ultimately lethal phase. However, disease progression is inhibited if the circulating corticosterone level is maintained at levels seen during the initial phase of disease. The effect of hypothalamic-pituitary-adrenocortical axis desensitization on the clinical course of experimental autoimmune encephalomyelitis is aggravated by a marked reduction in proinflammatory cytokine synthesis in the central nervous system in the later stages of disease, reflecting an increasing involvement of antibody, rather than T cell-dependent effector mechanisms, in disease pathogenesis, with time. Thus, our data indicate that distinct immune-endocrine effects play a decisive role in determining disease progression in multiple sclerosis, a concept supported by reports that a subpopulation of multiple sclerosis patients shows evidence of hypothalamic-pituitary-adrenocortical axis desensitization.

Animals↗
PubMed2005

Reverse transcriptase-polymerase chain reaction to detect avian encephalomyelitis virus.

A reverse transcriptase-polymerase chain reaction (RT-PCR) was developed and optimized for the detection of avian encephalomyelitis virus (AEV). A pair of primers was prepared based on the VP2 gene of the structural protein P1 region of the AEV genome. An avian encephalomyelitis virus-specific 619-base pair cDNA product was amplified by these primers from five reference/field strains of AEVs but not from 10 other avian pathogenic viruses and bacteria. The RT-PCR assay developed in this study was found to be sensitive and specific with as little as 10 pg of avian encephalomyelitis virus RNA detected using gel electrophoresis. Furthermore, AEV-RT-PCR was able to detect AE virus from chicken embryo brain at 3 days postinoculation as compared with the AE agar gel precipitation test (AGP), which required up to 11 days of incubation in the embryos.

Animals↗
PubMed2002

Encephalomyelitis disseminata: a rare, but challenging differential diagnosis of anorectic disorder.

The frequent occurrence of psychiatric syndromes in encephalomyelitis disseminata is known to obscure its diagnosis. We here report on the case of a 19-year-old female patient presenting symptoms of anorexia nervosa and subsequently diagnosed as suffering from encephalomyelitis disseminata. High dose corticoid treatment resulted in a nearly complete remission of the neurological symptoms as well as the normalization of her eating behaviour. Our case report underscores the importance of considering 'organic' aetiology in patients with symptoms of distinct eating disorders. The clinical course confirms recent findings, suggesting that acute inflammation in encephalomyelitis disseminata may induce behavioural symptoms, which precede the onset of neurological signs. To our knowledge, only one previous case has been reported to date.

Adult↗
PubMed2001

Roles of TNF-related apoptosis-inducing ligand in experimental autoimmune encephalomyelitis.

TRAIL, the TNF-related apoptosis-inducing ligand, induces apoptosis of tumor cells, but not normal cells; the roles of TRAIL in nontransformed tissues are unknown. Using a soluble TRAIL receptor, we examined the consequences of TRAIL blockade in an animal model of multiple sclerosis. We found that chronic TRAIL blockade in mice exacerbated experimental autoimmune encephalomyelitis induced by myelin oligodendrocyte glycoprotein. The exacerbation was evidenced primarily by increases in disease score and degree of inflammation in the CNS. Interestingly, the degree of apoptosis of inflammatory cells in the CNS was not affected by TRAIL blockade, suggesting that TRAIL may not regulate apoptosis of inflammatory cells in experimental autoimmune encephalomyelitis. By contrast, myelin oligodendrocyte glycoprotein-specific Th1 and Th2 cell responses were significantly enhanced in animals treated with the soluble TRAIL receptor. Based on these observations, we conclude that unlike TNF, which promotes autoimmune inflammation, TRAIL inhibits autoimmune encephalomyelitis and prevents activation of autoreactive T cells.

Animals↗
PubMed2004

MHC class II isotype- and allele-specific attenuation of experimental autoimmune encephalomyelitis.

Most autoimmune diseases are associated with certain MHC class II haplotypes. Autoantigen-based specific immune therapy can lead either to beneficial or, in the context of inflammatory conditions, detrimental outcomes. Therefore, we designed a platform of peptides by combinatorial chemistry selected in a nonbiased Ag-independent approach for strong binding to the rat MHC class II isotype RT1.D(n) allelic product of the RT1(n) haplotype that is presenting autoantigen in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis in LEW.1N rats. Peptide p17 (Ac-FWFLDNAPL-NH(2)) was capable of suppressing the induction of and also ameliorated established experimental autoimmune encephalomyelitis. MHC class II isotype and allele specificity of the therapeutic principle were demonstrated in myelin basic protein-induced experimental autoimmune encephalomyelitis in LEW rats bearing the RT1(l) haplotype. A general immunosuppressive effect of the treatment was excluded by allogeneic heart transplantation studies. In vitro studies demonstrated the blocking effect of p17 on autoantigenic T cell responses. We thus demonstrate a rational design of strong MHC class II-binding peptides with absolute isotype and allele specificity able to compete for autoantigenic sequences presented on disease-associated MHC class II molecules.

Alleles↗
PubMed2005

Resolution of a 16.8-Mb autoimmunity-regulating rat chromosome 4 region into multiple encephalomyelitis quantitative trait loci and evidence for epistasis.

To investigate effects of a 16.8-Mb region on rat chromosome 4q42-43 on encephalomyelitis, we performed a high-resolution mapping using a 10th generation advanced intercross line between the susceptible DA strain and the MHC identical but resistant PVG.1AV1 strain. Clinical signs of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis (EAE) developed in 29% of 772 F(10) rats. Three regions controlling disease, Eae20, Eae21, and Eae22, were mapped using 15 microsatellite markers spanning 16.8 Mb. Eae20 was a major genetic determinant within the region whereas Eae21 modified disease severity. Eae22 was identified as an epistatic region because it only displayed an effect together with Piebald Virol Glaxo (PVG) alleles on Eae20. Disease down-regulation by PVG alleles in the telomeric part of Eae20 was also demonstrated in DA rats made congenic for a approximately 1.44-Mb chromosomal region from PVG. As the region containing Eae20-Eae22 also regulates arthritis, together with the fact that the syntenic mouse 6F(2)-F(3) region regulates experimental lupus and diabetes, and the syntenic human 12p13.31-13.2 region regulates multiple sclerosis and rheumatoid arthritis, the present data point to genes that control several inflammatory diseases. The pairscan analyses of interaction, which here identified Eae22, are novel in the encephalomyelitis field and of importance in the design of further studies of this region in other diseases and species. The limited number of genes identified in Eae20, Eae21, and Eae22 enables focused examination of their relevance in mechanistic animal studies and screening of their association to human diseases.

Animals↗
PubMed1988

A rapid dot immunoassay for the detection of serum antibodies to eastern equine encephalomyelitis and St. Louis encephalitis viruses in sentinel chickens.

A dot enzyme-linked immunosorbent assay utilizing a novel membrane, polyvinylidene difluoride, is described. This assay was developed for the rapid detection of serum antibodies to eastern equine encephalomyelitis virus and St. Louis encephalitis virus in sentinel chickens. Antigens were spot-filtered through the membrane. Membranes were dipped into small vials of sera. Antigen-antibody complexes were detected with enzyme-conjugated antiglobulin which, when exposed to substrate, produced a colored insoluble product. The antibody detection protocol was completed within 50 min and was compared with a standard plate enzyme immunoassay. Chickens were experimentally infected with eastern equine encephalomyelitis and St. Louis encephalitis and bled on a daily basis. The dot immunoassay correctly identified 99% (123/124) of the eastern equine encephalomyelitis virus and 100% (67/67) of the St. Louis encephalitis virus antisera. Sera from sentinel chicken flocks in Maryland were also assayed. These data indicate that the dot immunoassay should be considered as an alternative to current assays for the screening of sera for antibodies to virus antigens. This assay could easily be performed in the field and allows for the screening of antibodies to several different viruses in one test.

Alphavirus↗
PubMed1977

Encephalomyelitis induced by canine distemper virus in non-human primates.

A strain of canine distemper virus was shown to be highly neuro-virulent in non-human primates. Intracerebral inoculation induced in monkeys histological lesions of encephalomyelitis, i.e., degenerative changes consisting mainly of neuronal damage and inflammatory changes such as perivascular cuffings and glial proliferation, in wide areas in the brain and spinal cord. In one monkey observed for 70 days, lesions with a tendency of subacute sclerosing were also noticed. Immunosuppression with cyclophosphamide or antithymocyte serum was found to aggravate the clinical course and to modify the histological lesions in the central nervous system as well as the level of antibody response to the virus in cerebrospinal fluid. Possible application of distemper encephalomyelitis in monkeys as a primate model for analysis of the immune mechanism involved in paramyxovirus-induced encephalomyelitis was discussed.

Animals↗
PubMed1976

[Comparative study of infectious and atypical encephalomyelitis in birds].

Studied were morphologically a total of 234 birds for infectious encephalomyelitis (IE) and atypic encephalomyelitis (AE) of which 70 were experimentally infected with standard reference strains of IE (Calnek 1143-42 birds, and Van Roeckel 28 birds), 32 were infected with a brain suspension of affected with AE birds, and 110 were spontaneously affected with AE. Those of the birds that were infected with the standard strains of IE as well as with the brain suspension exhibited changes in the central nervous system in the form of a non-suppurative encephalomyelitis, and in the viscera--lymphoidcell proliferations. These alterations proved analogous with those observed in birds spontaneously affected with AE. The changes in CNS in the case of IE were localized in the brain and the spinal cord, while the lesions in the case of AE were found chiefly in the brain. In AE there were perivascular lymphoidcell were groupings along the peripheral nerves. It was concluded that the histologic changes established may well serve to differentiate IE from AE in Marek's disease, the transitional paralysis, the Newcastle disease, and the alimentary encephalomalacia.

Animals↗
PubMed2001

Habitat preference of host-seeking Coquillettidia perturbans (Walker) in relation to birds and eastern equine encephalomyelitis virus in New Jersey.

Coquillettidia perturbans (Walker) has been implicated as a bridge vector of eastern equine encephalomyelitis virus in North America. Eastern equine encephalomyelitis virus epizootics occur regularly in wild birds in New Jersey with little or no involvement of susceptible dead end hosts even though high populations of Cq. perturbans are present. Several factors may limit eastern equine encephalomyelitis (EEE) virus transfer from birds to mosquito bridge vectors like Cq. perturbans (Walker), including bird/mosquito density, differences in bird/mosquito habitat preference, mosquito host preference, mosquito host-seeking behavior and mosquito avoidance behavior by birds. Our investigations focused on the host-seeking activities of Cq. perturbans at Colliers Mills Wildlife Management Area in Ocean County, New Jersey. We first examined the abundance of host-seeking Cq. perturbans at a height of 1.0 m in each of three habitats: forest, open field and marsh. We collected significantly more mosquitoes in the forest as compared to the marsh. Forest and field collections did not differ significantly from one another nor did field and marsh. Second, we examined the temporal and vertical distribution of host-seeking Cq. perturbans in a sylvan habitat at three heights (1.0, 2.5, and 6.0 m) from dusk to dawn. We found that Cq. perturbans did significantly more host-seeking during the night period than either the evening or morning. Host-seeking mosquitoes also tended to stay near the ground and at no time did they ascend into the forest canopy. Host-seeking Cq. perturbans and their apparent spatial disparity to roosting/nesting birds are discussed as a possible barrier to the transmission of EEE virus in New Jersey.

Animals↗
PubMedDate not supplied

[Can acute disseminated encephalomyelitis progress in a deferred way?].

OBJECTIVE: To report on the heterogeneity with regard to the clinical course of the acute disseminated encephalomyelitis (ADEM). CASE REPORT: A 5 year old boy suffered of acute disseminated encephalomyelitis of unknown origin. This child suffered two episodes of different neurologic symptoms separated by several weeks. Based on the clinical manifestations and typical appearance of magnetic resonance imaging findings and the absence of oligoclonal bands in CSF immunoglobulins, multiple sclerosis (MS) was ruled out. CONCLUSION: We postulate that the recurrent symptoms in our patient could be explained as a multiphasic disseminated encephalomyelitis (MDEM). Favourable outcome after simultaneous treatment with methylprednisolone and intravenous immunoglobulin is emphasized in this report.

Anti-Inflammatory Agents↗
PubMed2006

[A case of difficulty for differential diagnosis between encephalitis and acute disseminated encephalomyelitis].

A seventy-four-male with disorientation and convulsion was transferred to this hospital after three days fever which was unknown origin. Because the examination of cerebrospinal fluid were; cell count 1,560/3 (N : L = 4 : 1), protein 305 mg/dl, sugar 91 mg/dl, he was treated as encephalitis. However, MRI of the 18th hospital day revealed bilateral thalamic lesion and disseminated white matter lesions, suggesting acute disseminated encephalomyelitis. He left dementia after treatment and transferred to another hospital. Since, it is difficult to make a differential diagnosis between encephalitis and acute disseminated encephalomyelitis, early establishment of diagnostic criteria for acute disseminated encephalomyelitis is required.

Aged↗
PubMed1986

Ia expression in chronic relapsing experimental allergic encephalomyelitis induced by long-term cultured T cell lines in mice.

Chronic relapsing experimental allergic encephalomyelitis was induced in SJL mice by adoptive transfer of long-term cultured T cell lines. The T cells which were activated with myelin basic protein (MBP) derived from various species, all induced chronic relapsing experimental allergic encephalomyelitis with a similar high incidence. During the relapsing stage, lymphocytes obtained from the spleen responded well to MBP and were capable of transferring experimental allergic encephalomyelitis, whereas thymus lymphocytes did not respond to MBP. There was no difference in the proliferative response of splenocytes to MBP when splenocytes were isolated either from mice with clinical relapse or from mice that did not relapse. Pathological examination revealed a transient appearance of inflammatory cells during the acute stage. Similar cell infiltrates were also observed at the relapsing stage. The I-region associated (Ia) antigens appeared on vessels and astrocytes in the acute inflammatory lesions which coincided with the appearance of inflammatory cell infiltrates. Ia antigen expression diminished with the disappearance of inflammatory cells. During the relapsing stage, the Ia antigens were also expressed on the vessels and astrocytes in the fresh lesions. Our data indicate that MBP-reactive T cells persist at least in the spleen, for a long time. They may be reactivated by certain mechanisms probably in the central nervous system associated with the Ia-antigen expression, which facilitates the effector phase again. The initial event that triggers the Ia-expression is not known as yet.

Acute Disease↗
PubMed1987

Chronic relapsing necrotizing encephalomyelitis produced by myelin basic protein in mice.

Chronic relapsing experimental autoimmune encephalomyelitis is commonly seen in a number of species after a single injection of whole white matter in adjuvant but not after inoculation with myelin basic protein, the major encephalitogen of central myelin. In the present report on large groups of SJL mice, we describe a form of chronic relapsing experimental autoimmune encephalomyelitis with destructive lesions after a single inoculation of myelin basic protein in complete Freund's adjuvant. This condition was studied for up to 19 months postinoculation and was characterized by a relapsing-remitting or a chronic progressive course, usually with a prolonged latent period. Higher doses of 400 and 800 micrograms of myelin basic protein were more effective in inducing this condition than were lower doses of 100 and 200 micrograms. Large lesions were apparent in the white matter. These comprised widespread destruction and Wallerian degeneration with some demyelination towards the margins. Demyelination was an initial, albeit transient, event which was subsequently masked by nerve fiber destruction. Polymorphonuclear leukocytes were early and prominent components of the inflammatory infiltrate and together with macrophages appeared to be involved in the lysis of myelin and axons. Thus, despite the clinical similarities, these features contrast the model with the more purely demyelinative lesions of chronic relapsing experimental autoimmune encephalomyelitis in other species and multiple sclerosis in man.

Adjuvants, Immunologic↗
PubMed1988

A synthetic peptide from myelin proteolipid protein induces experimental allergic encephalomyelitis.

Immunization of animals with proteolipid protein, the major protein constituent of central nervous system myelin, produces experimental allergic encephalomyelitis. The goal of the present study was to identify an encephalitogenic determinant of this protein. For this purpose, SWR mice were immunized with five groups of pooled synthetic peptides corresponding to various regions of the myelin proteolipid protein sequence. Clinical EAE was observed in only one group. Inguinal lymph node cells from animals in this group responded ([3H]thymidine incorporation) to a peptide within the pool containing residues 103-116 YKTTICGKGLSATV. Mice subsequently immunized with 50 nmol of this peptide developed severe EAE within 3 wk, and their T cell-enriched inguinal lymph node cells responded specifically to this peptide. Control mice immunized to proteolipid peptide 202-217 DARMYGVLPWNAFPGK did not develop experimental allergic encephalomyelitis, and their inguinal lymph node cells were unresponsive to either peptide. Thus, a peptide corresponding to a sequence within the proteolipid protein can produce classical acute experimental allergic encephalomyelitis. This is the first report of a synthetic encephalitogenic peptide from myelin proteolipid protein.

Amino Acid Sequence↗