Detection of serum antibody against arrestin from patients with acute disseminated encephalomyelitis.
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In our previous study, we found the presence of serum autoantibody against arrestin in patients with multiple sclerosis (MS), while such serum autoantibody was not detected from patients with other neurological diseases and control subjects. We suggested that serum arrestin antibody titers may be useful for the diagnosis and evaluation of the disease's course. In the present study we examined sera from 7 patients, who were initially diagnosed as having acute disseminated encephalomyelitis (ADEM), for the presence of serum antibody against arrestin, in order to study the specificity of the serum antibody among demyelinated diseases. High titers were detected from 2 patients out of 7. One of the patients, a 4 year-old girl, presented with an additional neurological attack during the 6 months after the initial attack, resulting in change of diagnosis to MS. During her disease course the serum titers against arrestin fluctuated in correspondence with the disease's activity. These observations suggest that the presence of serum autoantibody against arrestin may be specific to MS and be helpful for differential diagnosis of ADEM and MS. (+info)
Acute disseminated encephalomyelitis (ADEM) after autologous peripheral blood stem cell transplant for non-Hodgkin's lymphoma.
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Acute disseminated encephalomyelitis (ADEM) is a demyelinating disorder of the central nervous system with an acute clinical onset and a wide variability in severity and outcome. It usually follows a viral infection or an immunization and is thought to be immuno- mediated. We report a case of ADEM with a dramatic clinical onset in an autologous peripheral blood stem cell transplant (PBSCT) recipient for non-Hodgkin's lymphoma who developed the neurologic syndrome 12 days after PBSC reinfusion. This is the first report of ADEM in the setting of autologous PBSCT, a therapeutic procedure performed with increasing frequency in a wide variety of hematologic and solid malignancies. (+info)
Acute disseminated encephalomyelitis after parenteral therapy with herbal extracts: a report of two cases.
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Two patients with acute disseminated encephalomyelitis after repeated injection of extracts from several different plants are described. There was no evidence of prior infection or vaccination. Both patients recovered rapidly after treatment with methylprednisolone. Acute disseminated encephalomyelitis should be considered a rare complication of parenteral therapy with herbal extracts. (+info)
Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children.
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Forty-eight children with disseminated demyelination of the CNS, 28 with acute disseminated encephalomyelitis (ADEM), seven with multiphasic disseminated encephalomyelitis (MDEM) and 13 with multiple sclerosis were studied for a mean follow-up period of 5.64 years. The presentation findings of the ADEM/MDEM group were compared with those of the multiple sclerosis group. The following findings were more commonly seen in ADEM/MDEM presentation compared with the multiple sclerosis presentations: predemyelinating infectious disease (74 versus 38%, P: < 0.05); polysymptomatic presentation (91 versus 38%, P: < 0.002); pyramidal signs (71 versus 23%, P: < 0.01); encephalopathy (69 versus 15%, P: < 0.002); and bilateral optic neuritis (23 versus 8%, not significant). Seizures occurred only in the ADEM/MDEM group (17 versus 0%, not significant). Unilateral optic neuritis occurred only in the multiple sclerosis patients (23 versus 0%, P: < 0.01). There were no differences in the frequencies of transverse myelitis, brainstem involvement, cerebellar signs and sensory disturbance between the two groups. ADEM/MDEM patients were more likely to have blood leucocytosis (64 versus 22%, P: < 0.05), CSF lymphocytosis (64 versus 42%, not significant) and CSF protein elevation (60 versus 33%, not significant). Patients presenting with multiple sclerosis were more likely to have intrathecal synthesis of oligoclonal bands on presentation (64 versus 29%, not significant). MRI showed that subcortical white matter lesions were almost universal in both groups, though periventricular lesions were more common in multiple sclerosis (92 versus 44%, P: < 0.01). By contrast, in ADEM/MDEM there was absolute and relative periventricular sparing in 56 and 78% of patients, respectively. Follow-up MRI revealed complete or partial lesion resolution in 90% and no new lesions in the ADEM/MDEM group. All of the multiple sclerosis patients had new lesions on repeat MRI (five during relapse and six during asymptomatic convalescent phases). The outcome in the ADEM patients was mixed; 57% of patients made a complete recovery. The mean follow-up for the 35 ADEM/MDEM patients was 5.78 years (range 1.0-15.4 years). Eight of the 13 multiple sclerosis patients relapsed within the first year; 11 had a relapsing-remitting course, one a primary progressive course and one a secondary progressive course. These differences in the presentation of ADEM/MDEM compared with multiple sclerosis may help in the prognosis given to families regarding the possibility of later development of multiple sclerosis. (+info)
Acute disseminated encephalomyelitis developed after acute herpetic gingivostomatitis.
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A child with acute disseminated encephalomyelitis (ADEM) developed after acute herpetic gingivostomatisis was described. Inspite of the improvement of his gingivostomatitis, his consciousness gradually deteriorated and he was admitted to Nakadori General Hospital. His consciousness level was drowsiness and increased bilateral patellar reflexes were shown. Because magnetic resonance imaging (MRI) T2-weighted scan showed areas of high signal intensity disseminated in superior portion of medulla oblongata, dorsal portion of pons, basal nuclei and thalamus, he was suspected as having ADEM. Anti-herpes simplex virus (HSV) 1 IgG and IgM antibodies elevated in both blood and cerebrospinal fluid. From these results, HSV1 infection was thought to be the preceding infection of ADEM. Methylprednisolone therapy (20 mg/kg daily) for 3 days, followed by prednisolone (2 mg/kg) was started, with an excellent response. In addition, administration of acyclovir was also continued, considering the complication of HSV encephalitis. MRI T2-weighted scan performed at 2 months later after the onset of ADEM revealed disappearance of the lesions. He was discharged without remaining disorders. It is difficult to distinguish between ADEM and HSV encephalitis because both of these diseases show various neurological symptoms. In our case, MRI was the most useful method for correct diagnosis of ADEM. We concluded that ADEM is important as a disease of central nervus system due to HSV1 infection, in addition to encephalitis. (+info)
Delayed MR imaging changes in acute disseminated encephalomyelitis.
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BACKGROUND AND PURPOSE: White matter lesions on MR images obtained from patients with acute disseminated encephalomyelitis (ADEM) have been reported to appear shortly after symptom onset, and their resolution has been claimed to parallel recovery. To elucidate the temporal evolution of these lesions and to associate the changes on MR images to the patients' clinical condition, we performed serial MR imaging on patients with ADEM. METHODS: Several consecutive T2-weighted and fluid-attenuated inversion recovery scans were obtained from four previously healthy adult patients with ADEM within the first days after the onset of symptoms and again during the recovery period. MR imaging was done first on a weekly to biweekly basis and later at 1- to 2-month intervals for up to 8 months. RESULTS: MR scans of three of these patients did not show any specific abnormalities until several weeks after the onset of the disease. As the lesions later appeared, their number increased during the recovery period. CONCLUSION: MR imaging performed during the first days after the onset of the disease may not reveal any pathologic findings. The appearance of the ADEM-associated MR imaging changes may be associated with recovery rather than decline. It remains to be studied whether the new MR imaging techniques reveal the lesions associated with ADEM faster than the conventional T2-weighted imaging. (+info)
Quantitative proton MR spectroscopic imaging in acute disseminated encephalomyelitis.
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Serial MR imaging and quantitative proton MR spectroscopic imaging (MRSI) findings of a 4-year-old boy with acute disseminated encephalomyelitis (ADEM) are reported. Over a 2-month period characterized by an initial illness and two relapses, each with full recovery, MR imaging exhibited the appearance and disappearance of multifocal lesions throughout the CNS that correlated only partly with the neurologic impairment. During one relapse, MRSI revealed low levels of N-acetylaspartate (NAA) within the regions of prolonged T2 signal intensity. All other metabolites were normal. At follow-up, the MR imaging and MRSI abnormalities had fully resolved. MRSI might play an important role in the diagnosis of ADEM, as well as in the elucidation of underlying pathophysiologic processes in this poorly defined disorder of children. This case demonstrates that reduced levels of NAA are not always associated with neuronal loss, irreversible tissue damage, or poor neurologic outcome. (+info)
Heat shock protein 60 in corpora amylacea.
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Heat shock protein 60 representation in the corpora amylacea of the brain was investigated in five different neurological diseases. In the cases with cerebral infarct, amyotrophic lateral sclerosis, multiple sclerosis, acute disseminated encephalomyelitis and primary tumors of the nervous system the corpora amylacea showed similar appearance with strong HSP-60 positivity in all investigated disorders at the predilection sites. In the inflammatory diseases, besides corpora amylacea, several cellular elements exhibited HSP-60 immunostaining too. In these cases, the widespread HSP-60 immunoreactivity associated with relative moderate corpora amylacea production as compared to other diseases. From this contradiction we concluded the corpora amylacea participate in the cellular stress reaction but stress protein synthesis certainly is not the primary event in corpora amylacea formation. In the development of the corpora amylacea the incipient process is most probably degenerative in nature, which later on is accompanied by stress protein synthesis and slow growing of these round structures designated for a protective role in the brain. However, the role of the stress protein synthesis in the corpora amylacea formation and growth was not unequivocally answered in this study. It is necessary to perform further comparative investigations of the stress protein representation and corpora amylacea formation in different diseases which may help in discovering useful pathogenetic data and the biological role of this degenerative structure. (+info)