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PubMed2002

Encephalomyelitis due to human parechovirus type 1.

OBJECTIVES: The implication of a viral agent in encephalomyelitis has been reported for several years. In the present study we wanted to demonstrate the presence of human parechovirus type 1 (HPEV1) in a patient diagnosed with encephalomyelitis. STUDY DESIGN: Clinical samples (throat and rectal swabs, acute and convalescent sera, cerebrospinal fluid) were collected from a 10-month-old boy diagnosed with encephalomyelitis. The appropriated samples were tested for cytomegalovirus, varicella zona virus, mumps virus and enteroviruses with specific culture, and serological and molecular biological techniques. RESULTS: HPEV1 was isolated from the throat and its genome was additional detectable in the cerebrospinal fluid, throat swab and acute serum. The samples were negative for all other tested viruses. CONCLUSION: To our knowledge, this is the first reported case of HPEV1 infection related to encephalomyelitis. This emphasis that human parechoviruses can be responsible for severe central nervous system infections in children.

Cerebrospinal Fluid↗
PubMed1984

Measles encephalomyelitis--clinical and immunologic studies.

We studied 19 patients with postinfectious encephalomyelitis complicating natural measles-virus infections, and our results support the hypothesis that this demyelinating disease has a pathogenesis similar to that of experimental allergic encephalomyelitis. Early myelin destruction was demonstrated by the presence of myelin basic protein in cerebrospinal fluid, and lymphocyte proliferative responses to myelin basic protein were found in 8 of 17 patients tested. A lack of intrathecal synthesis of antibody against measles virus suggests that measles encephalomyelitis may not be dependent on virus replication within the central nervous system. Similar lymphoproliferative responses to myelin basic protein of lymphocytes from single patients with encephalomyelitis after rabies vaccine or after varicella or rubella virus infections suggest a common immune-mediated pathogenesis for the perivenular demyelinating disease that can follow the injection of neural tissues or infection by a variety of viruses.

Adolescent↗
PubMed1991

T-cell receptor peptide immunization leads to enhanced and chronic experimental allergic encephalomyelitis.

It has previously been reported that synthetic peptides corresponding to sequences derived from T-cell receptor variable regions identified as dominant in the T-cell-mediated autoimmune disease experimental allergic encephalomyelitis in both the mouse and the rat can down-regulate disease in Lewis rats. In contrast to these results, we have found that immunization of Lewis rats with such peptides in complete Freund's adjuvant prior to induction of experimental allergic encephalomyelitis with myelin basic protein leads to responses ranging from profound disease enhancement to lack of disease. In some cases, enhanced disease was followed by a prolonged neurologic deficit that resembles multiple sclerosis more closely than does acute experimental allergic encephalomyelitis. These findings, on the one hand, support previous results showing T-cell receptor peptide-induced modulation of the disease experimental allergic encephalomyelitis and, on the other, indicate that such immunization is not a reliable method for inducing suppression of encephalitogenic effector cells.

Amino Acid Sequence↗
PubMed1987

The pathogenesis of acute viral encephalitis and postinfectious encephalomyelitis.

Japanese encephalitis and postmeasles encephalomyelitis represent two important forms of acute encephalitis in the developing world. Japanese encephalitis accounts for 20,000 acute illnesses per year, and measles encephalomyelitis accounts for as many as 100,000. Both are accompanied by mortalities of 20%-30%, and in both forms, approximately one-half of the survivors have neurological sequelae. Therefore, these two diseases are responsible for a considerable proportion of worldwide mental and motor disabilities. Furthermore, both diseases are preventable with use of safe vaccines. Despite these similarities, their very different pathologies appear to be based on different mechanisms of pathogenesis (table 2). In Japanese encephalitis there is direct invasion of the virus into the nervous system, selective infection and destruction of neurons, and evidence that both humoral and cellular immune responses attenuate the infection. In measles encephalomyelitis there is little evidence that the virus invades the nervous system. Rather, measles virus infects lymphoid cells and causes abnormalities in immune regulation. Humoral immune responses are not found within the nervous system, and the cellular immune response may be inappropriately directed against host antigens. In measles encephalomyelitis, the inflammatory cells entering the nervous system may be the effector cells of autoimmune disease.

Animals↗
PubMed1998

Review of 23 patients affected by the stiff man syndrome: clinical subdivision into stiff trunk (man) syndrome, stiff limb syndrome, and progressive encephalomyelitis with rigidity.

OBJECTIVE: To investigate whether the stiff limb syndrome may be separated from the stiff man syndrome and progressive encephalomyelitis with rigidity on simple clinical grounds, and whether such a distinction has implications for aetiology, treatment, and prognosis. METHODS: Twenty three patients referred over a 10 year period with rigidity and spasms in association with continuous motor unit activity, but without evidence of neuromyotonia, extrapyramidal or pyramidal dysfunction or focal lesions of the spinal cord were reviewed. The patients were divided into those with an acute or subacute illness, leading to death within 1 year, and those with a chronic course. The latter were divided into those in whom rigidity and spasms dominated in the axial muscles, or in one or more distal limbs, at the time of their first assessment. RESULTS: This simple division identified three distinct groups of patients. (1) Progressive encephalomyelitis with rigidity: two patients had a rapidly progressive condition characterised by widespread rigidity which resulted in death within 6 and 16 weeks. One patient had negative anti-GAD and anti-neuronal antibodies, but had markedly abnormal CSF and widespread denervation. The principal pathological findings in this case were a subacute encephalomyelitis which primarily affected the grey matter. In the remaining patient anti-GAD antibodies were not tested, and postmortem was refused. (2) Stiff man syndrome: eight patients had rigidity and painful spasms of the lumbar paraspinal, abdominal, and occasionally proximal leg muscles associated with a lumbar hyperlordosis. There was no involvement of the upper limbs, distal lower limbs, sphincters or cranial nerves. Seven had anti-GAD antibodies and most had additional evidence of autoimmune disease. Neurophysiologically there was continuous motor unit activity with abnormal exteroceptive reflexes, but a normal interference pattern during spasms. The patients all responded to baclofen/diazepam and remained ambulant. (3) Stiff limb syndrome: thirteen patients had rigidity, painful spasm, and abnormal postures of the distal limb, ususphincter or brainstem involvement. Generalised myoclonic jerks were not a feature. Only two had truncal rigidity, and another two had anti-GAD antibodies. Most had no evidence of autoimmune disease. Neurophysiologically they had continuous motor unit activity in the affected limb, abnormal exteroceptive reflexes, and abnormally segmented EMG activity during spasms. The disease ran a protracted course, and most patients had only a partial response to baclofen or diazepam. About half became wheelchair bound. CONCLUSIONS: The stiff limb syndrome seems distinct from the stiff man syndrome or progressive encephalomyelitis with rigidity, and is an important cause of rigidity and spasm in the setting of continuous motor unit activity.

Adult↗
PubMed1985

Anti-myelin basic protein antibody in experimental allergic optic neuritis and encephalomyelitis.

We produced demyelinating optic neuritis and encephalomyelitis in juvenile strain 13 guinea pigs by sensitization with optic nerve myelin. Three distinct clinical courses were noted: a severe, acute optic neuritis associated with a rapidly fatal encephalomyelitis; a mild, chronic optic neuritis with a nonfatal encephalomyelitis; and an initially mild disease followed by an acute exacerbation of optic neuritis and fatal encephalomyelitis. Clinically mild disease was associated with elevated levels of anti-myelin basic protein antibody, while severe disease was associated with extremely low antibody levels.

Animals↗
PubMed2006

Acute disseminated encephalomyelitis in North Indian children: clinical profile and follow-up.

Acute disseminated encephalomyelitis in children is not uncommon in developing countries, yet there is little systematic documentation of its clinical profile and follow-up. We studied the clinical and neuroradiologic features of acute disseminated encephalomyelitis in 52 consecutive children. Clinical details, magnetic resonance imaging (MRI) findings, and the results of other investigations were recorded, and children were followed up from 6 to 48 months. A repeat MRI was done after 3 to 4 months, and in those with persistent lesions, another MRI was done after 6 to 7 months of discharge. The mean age at presentation was 6.14 +/- 3.17 years, 73.1% were male, and 17 children had a history of antecedent infectious illness or vaccination. Most children had a meningoencephalitic presentation, with sudden-onset motor weakness in 76.9% and seizures in 36.5%. Altered sensorium and pyramidal signs were seen in 55.8% and 80.7% of children, respectively. On MRI, scattered T(2)-weighted hyperintense lesions were seen, mainly in the subcortical white matter, especially in the parietal (53.8%) and frontal (30.17%) regions. Thalamic, basal ganglia, and callosal lesions were seen in 30.76%, 17.3%, and 13.46% of cases, respectively. Variable contrast enhancement was seen in 48% of those who had contrast MRIs. The response to methylprednisolone was good, with dramatic recovery in 26.9% and marked improvement in 51.9% at discharge. On follow-up, of 44 children, residual smaller MRI lesions were seen in 30. The MRI was repeated at 6 months in children with residual lesions, and it was found that the lesions either disappeared or were significantly reduced after 6 months in 75% of cases. Four children had relapse of acute disseminated encephalomyelitis with new lesions on MRI. All of them responded to methylprednisolone. None of the clinical or neuroradiologic factors at presentation had any significant correlation with relapse. Six months after discharge, no deficits could be found in 61.3% of cases; 15.9% and 4.5% had motor and cognitive deficits, and 9% had multiple deficits. The presentation of pediatric acute disseminated encephalomyelitis in developing countries is similar to that in developed countries. In spite of an aggressive presentation, most children respond well to corticosteroids. MRI lesions disappear or are significantly reduced at 6 months in the majority of cases.

Brain↗
PubMed2002

Acute disseminated encephalomyelitis: a long-term follow-up study of 84 pediatric patients.

BACKGROUND: Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disease of the CNS. Few pediatric series have been published, with retrospective and short-term follow-up studies. OBJECTIVES: To describe a cohort of pediatric patients with ADEM and to determine whether clinical and neuroimaging findings predict outcome. METHODS: A prospective study was conducted between March 1988 and July 2000 on 84 consecutive children with ADEM at the National Pediatric Hospital "Dr. J. P. Garrahan." RESULTS: Mean age at onset was 5.3 +/- 3.9 years, with a significant male predominance. Sixty-two patients (74%) had a preceding viral illness or vaccination. Acute hemiparesis (76%), unilateral or bilateral long tract signs (85%), and changes in mental state (69%) were the most prominent presenting features. Four MRI groups were identified: ADEM with small lesions (62%), with large lesions (24%), with additional bithalamic involvement (12%), and acute hemorrhagic encephalomyelitis (2%). Of the 54 children whose CSF samples were analyzed, none showed intrathecal oligoclonal bands. The use of high-dose corticosteroid treatment, particularly IV methylprednisolone, was associated with good recovery and resolution of MRI lesions. After a mean follow-up of 6.6 +/- 3.8 years, 90% of children showed a monophasic course, and 10% a biphasic disease. Eighty-nine percent of patients show at present Expanded Disability Status Scale scores of 0 to 2.5. Eleven percent have disability scores of 3 to 6.5. CONCLUSIONS: Childhood acute disseminated encephalomyelitis is a benign condition, affecting boys more frequently. No association was found between MRI groups and disability. Disability was related to optic nerve involvement at presentation. Even in relapsing cases, the distinction between acute disseminated encephalomyelitis and MS was possible on the basis of long-term clinical and neuroimaging follow-up and the absence of oligoclonal bands in CSF.

Adolescent↗
PubMed2005

Thymoquinone inhibits the activation of NF-kappaB in the brain and spinal cord of experimental autoimmune encephalomyelitis.

The present study was done to investigate the possible effects of thymoquinone on the inhibition of activation of NF-kappaB in experimental autoimmune encephalomyelitis in the rat model of multiple sclerosis. Experimental autoimmune encephalomyelitis was induced in Lewis rats by injecting myelin basic protein emulsified in complete freund's adjuvant. Several parameters including clinical signs, perivascular cuffing and infiltration of mononuclear cells in the brain and spinal cord, glutathione levels in the red blood cells and inhibition of the activation of NF-kappaB were determined to assess the degree of protection. The study showed that treatment of rats with thymoquinone 1 mg/kg/day concomitant to myelin basic protein and after the appearance of clinical signs resulted in preventing and ameliorating experimental autoimmune encephalomyelitis. Thymoquinone was able to counter perivascular cuffing and infiltration of mononuclear cells in the brain and spinal cord, increase the red blood cell glutathione, and inhibit the activation of NF-kappaB in the brain and spinal cord. These results were consistent with the clinical signs and suggest a beneficial effect of thymoquinone against experimental autoimmune encephalomyelitis in the rat model of multiple sclerosis.

Animals↗
PubMed1987

Comparative analysis of coronavirus JHM-induced demyelinating encephalomyelitis in Lewis and Brown Norway rats.

Lewis and Brown Norway rats were infected at different ages with the neurotropic murine coronavirus strain, JHM and the resultant central nervous system diseases were studied. Suckling rats of both strains came down with a fatal, acute encephalomyelitis. Weanling Lewis rats developed a subacute demyelinating encephalomyelitis which neuropathologically revealed changes of an immunopathologic reaction. In contrast, Brown Norway rats developed a clinically silent subacute demyelinating encephalomyelitis with a persistent JHM virus infection which was less severe and quite different from the subacute demyelinating encephalomyelitis in Lewis rats with respect to size, distribution, and localization of the demyelinating plaques as well as the type of infiltrating cells. In addition, infected Lewis rats showed a pronounced lymphocyte proliferation to myelin basic protein and JHM virus whereas lymphocytes from infected Brown Norway rats did not react to these two antigens. These observations demonstrate the pathogenetic importance of host factors in the development of virus-induced demyelination.

Aging↗
PubMed1989

Nondiscocytic erythrocytes in myalgic encephalomyelitis.

Blood samples from 102 volunteers who believed they suffered from myalgic encephalomyelitis were photographed in a scanning electron microscope at 500x. All identifiable cells were counted and classified on the basis of their shape. The frequency of each cell shape was expressed as a percentage of the total number of cells counted in the sample. The resulting data were compared with that from 52 healthy controls and 99 cases of multiple sclerosis which had been selected randomly by a computer from a panel of 229 cases in a concurrent study. Samples from subjects with myalgic encephalomyelitis had the lowest percentages of normal red cells and the highest incidence of cup forms. The results provide evidence that myalgic encephalomyelitis has an organic cause. Quantitative analysis of red cell shape may assist in the diagnosis of myalgic encephalomyelitis.

Adolescent↗
PubMed1981

Relapsing experimental allergic encephalomyelitis in the SJL/J mouse.

A single injection dose-response curve was done in the SJL/J mouse using varying amounts of syngeneic spinal cord homogenate and Mycobacterium tuberculosis H37RA in a Freund's type of adjuvant. Inoculation with as little as 0.025 mg. of cord homogenate induced severe experimental allergic encephalomyelitis in some mice. Possible reasons for the great ease of induction of experimental allergic encephalomyelitis with this single injection regimen in comparison with other single injection schemes are discussed. No single injection dose combination was found that induced severe experimental allergic encephalomyelitis in all of a group of mice. When two injections 1 week apart were given, all mice so injected developed severe experimental allergic encephalomyelitis, all had relapses, and nine of 10 had multiple relapses. The number of relapses and severity of residual neurologic deficits were much greater in the two-injection group than in the single injection group.

Animals↗
PubMed1980

Neuropathology of experimental allergic encephalomyelitis in inbred strains of mice.

Ten inbred strains of mice were tested for their susceptibility to experimental allergic encephalomyelitis (EAE) after sensitization with mouse spinal cord in complete Freund's adjuvant followed by booster injections of Bordetella pertussis. The results extended previous findings in that not all susceptible mice possessed the H-2s haplotype, but mice with an H-2q background (DBA1/J strain) were also susceptible. Neuropathologic examination of experimental allergic encephalomyelitis in the mouse showed that from strain to strain, the condition was similar. The over-all pathologic picture was somewhat midway between that seen in other species sensitized with whole nervous tissue in complex Freund's adjuvant and hyperacute experimental allergic encephalomyelitis in rats similarly sensitized but with the addition of B. pertussis. Perivascular cuffing, though present, was less pronounced than in other species. There was a prominent polymorphonuclear response, and extravasation of fibrin and red cells occurred. Primary demyelination was a transient, early feature of the disease process in mice, but nerve fiber depletion and gliosis occurred as the disease progressed. The observed myelin degradation most commonly involved the ingestion by macrophages of small fragments of dissociated myelin via crypts or infoldings of the cell surface, at the bases of which were pinocytic, coated vesicles. A similar pattern of myelin breakdown has been described in mouse hepatitis virus encephalomyelitis and multiple sclerosis.

Animals↗
PubMed1994

Deep gray matter involvement in children with acute disseminated encephalomyelitis.

PURPOSE: To review the frequency, distribution, and extent of deep gray matter disease in children with acute disseminated encephalomyelitis. METHODS: The MR examinations of 10 patients, who were discharged with the clinical diagnosis of acute disseminated encephalomyelitis between 1986 and 1992, were retrospectively reviewed. Locations of abnormal signal in the cerebral and cerebellar cortices, white matter, and deep gray matter nuclei were recorded. Precontrast and postcontrast images were compared, when available, to assess degree of enhancement (if any). RESULTS: Six patients had foci of prolonged T2 relaxation in the deep gray matter, ranging in size from less than 1 cm to 4 cm. The caudate heads were involved in 4 patients, caudate body in 3, globus pallidus in 3, putamina in 3, and thalami in 4. In 1 patient, the thalami were involved nearly symmetrically, with mild mass effect. Asymmetric subcortical white matter involvement was present as well. Prolonged T2 relaxation was present within the cerebral cortex in 4 patients and was associated with subcortical white matter abnormality in 3 and more central white matter disease in 1. Nine of 10 patients demonstrated foci of T2 prolongation in white matter, most commonly involving the subcortical region, corona radiata, and centrum semiovale. Three patients also had periventricular foci. Of the 3 patients receiving gadolinium, one showed no enhancement. Two of the patients showed enhancement of some but not all lesions. One patient, who had normal brain MR findings and symptoms of myelopathy, underwent spine MR which demonstrated focal linear areas of T2 prolongation in the spinal cord at levels C-1 to C-2 and T-6. CONCLUSION: Involvement of deep gray matter was common in our small series. The finding of T2 prolongation in these structures does not preclude the diagnosis of acute disseminated encephalomyelitis in the proper clinical setting. Because thalamic involvement is reported to be rare in multiple sclerosis, it may prove useful in distinguishing between acute disseminated encephalomyelitis and the initial presentation of multiple sclerosis.

Adolescent↗
PubMed1994

[Acute disseminated encephalomyelitis].

Acute disseminated encephalomyelitis (ADEM) follows certain viral infection or vaccinations, which has a close etiological relationship to experimental autoimmune encephalomyelitis (EAE). Immunological examinations have not been sufficiently carried out on human ADEM except postmeasles encephalomyelitis. The most important pathogenic role in ADEM might be changes of immune regulatory mechanisms by virus infection. Therefore, it would be very useful to investigate cytokine, adhesion molecules and receptors on neural cells and endothelial cells in the central nervous system. Recently, the incidence of postvaccinated encephalomyelitis has reduced. Neurologic complications of immunization have been still reported, however, there is no scientific method to prove that the association is causal or coincidental in an individual case.

Amino Acid Sequence↗
PubMed1997

[Acute disseminated encephalomyelitis].

Acute disseminated encephalomyelitis (ADEM) occurs late in the course of viral infection, mainly exanthematous diseases such as measles, chicken pox, and rubella. Postinfectious encephalomyelitis is characterized by immune-mediated demyelination, which is found in experimental autoimmune encephalomyelitis (EAE), and virus cannot be isolated from the central nervous system. The investigations using animal models infected with. Theiler's virus or measles virus would be very useful for clarifying the mechanisms of demyelination induced by viral infection. Although the incidence of postvaccinal encephalomyelitis has fallen markedly due to development of vaccines, the neurological complications following immunization are still reported. The vaccines prepared from viruses other than live-attenuated viruses and whole-killed organisms have never been proved to induce ADEM.

Animals↗
PubMed1978

Post-infectious encephalomyelitis: some aetiological mechanisms.

The possibility that acute disseminated encephalomyelitis (ADEM) and epidemic myalgic encephalomyelitis ('epidemic neuromyasthenia') may share a common pathogenesis is examined and many factors common to the two diseases are described. It is suggested that further study of ADEM may help our understanding of epidemic myalgic encephalomyelitis.

Diagnosis, Differential↗
PubMed2005

In vitro, melatonin treatment decreases nitric oxide levels in murine splenocytes cultured with the venezuelan equine encephalomyelitis virus.

The purpose of this work was to determine the effect of melatonin on the nitric oxide levels in murine splenocytes cultured with the Venezuelan equine encephalomyelitis virus. After incubation, nitric oxide levels were measured by the diazotization assay. Those cultures with the Venezuelan equine encephalomyelitis virus increased nitric oxide levels. Splenocytes infected and treated with 100 and 150 microg/ml of melatonin, decreased significantly the nitric oxide levels when compared to infected and non-treated splenocytes. These findings show that splenocytes infected with the Venezuelan equine encephalomyelitis virus generate important amounts of nitric oxide and suggest that melatonin protects the mice infected with the Venezuelan equine encephalomyelitis virus by a mechanism involving the decreasing of nitric oxide concentrations in tissue.

Animals↗