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PubMed2006

Rapid eye movement sleep behavior disorder and potassium channel antibody-associated limbic encephalitis.

Of six patients registered in our center with nonparaneoplastic limbic encephalitis associated with antibodies to voltage-gated potassium channels, the five men had rapid eye movement sleep behavior disorder (RBD) coincident with voltage-gated potassium channel antibody-associated limbic encephalitis onset. In three patients, immunosuppression resulted in resolution of RBD in parallel with remission of the limbic syndrome. RBD persisted in two patients with partial resolution of the limbic syndrome. Our findings suggest that RBD is frequent in the setting of voltage-gated potassium channel antibody-associated limbic encephalitis and can be related to autoimmune-mediated mechanisms. In addition, these observations suggest that impairment of the limbic system may play a role in the pathogenesis of RBD.

Aged↗

PubMed1977

Acute measles encephalitis of the delayed type.

An acute measles encephalitis with epilepsia partialis continua occurred three months after measles in a previously healthy child with no detectable immunological defect. Levels of measles antibodies in serum and cerebrospinal fluid were high, and tubular inclusions of the type seen in subacute sclerosing panencephalitis were found in nerve cell nuclei. A communicating high-pressure hydrocephalus developed in the later stage of the disease. This case demonstrates that measles encephalitis of the delayed type should systematically be considered in children with acute encephalitis.

Acute Disease↗

PubMed1981

Encephalitis after inhalation of measles virus: a pathogenetic study in hamsters.

A neuroadapted strain of measles virus (HNT) was administered by inhalation to newborn hamsters. Primary replication of virus in the lung was followed by the transient appearance of virus in spleen within 7 to 9 days of inoculation. A terminal encephalitis occurred between 6 and 60 days in 31% of infected hamsters, and virus was recovered by explant culture of these brains. Virus could not be cultured directly from brain or tissue homogenates. At least 7% of hamsters that had survived the infection for two months had antibody to measles virus. The histopathological change in morbid animals was limited to the central nervous system (CNS) and consisted of small foci of necrosis, perivascular mononuclear cell infiltrates, intracytoplasmic and intranuclear inclusions, and vacuolated pyknotic neurons. Immunofluorescent studies disclosed measles antigen in the lungs and brain. This hamster model of measles encephalitis following a "natural" route of inoculation appears to represent a faithful reproduction of certain CNS complications of natural measles infection in humans, i.e., measles encephalitis and subacute sclerosing panencephalitis.

Animals↗

PubMed1995

Genetic susceptibility to herpetic encephalitis of inbred rabbits of B/Jas strain.

Inbred rabbits of B/Jas strain were found to be highly susceptible to herpes simplex virus type 1 encephalitis, following i.v. injection of the virus, while Chbb:HM strain rabbits were not susceptible. The susceptibility trait seemed to be inherited recessively, involving multiple genes, because (B/Jas x Chbb:HM)F1 hybrids were as resistant as Chbb:HM rabbits, and because more than 90% of backcrosses of (B/Jas x Chbb:HM)F1 to B/Jas were resistant to viral inoculation. The encephalitis in B/Jas rabbits resembled human herpes simplex encephalitis, in that the temporal lobe as well as the brain stem were affected preferentially, leading to the development of various types of seizures, such as circling, loss of balance leading to a fall, and tonic and clonic convulsions. The disease could be diagnosed by magnetic resonance imaging (MRI) analysis before onset of seizures, and diseased rabbits showed a marked lymphopenia at onset of seizures.

Animals↗

PubMed1995

Adenovirus mixture isolated from the brain of an AIDS patient with encephalitis.

A mixture of adenoviruses 31 and 49 was isolated from the brain of an AIDS patient with encephalitis. Adenovirus hexon protein was detected in neurons by indirect immunofluorescence. By restriction endonuclease analysis both adenovirus 31 and 49 were shown to be new genotypes. This is the first report of the isolation of a mixture of adenoviruses from adenovirus encephalitis and the first association of adenovirus 49, a new candidate serotype, with encephalitis.

AIDS-Related Opportunistic Infections↗

PubMed1993

Nonverbal amnesia and asymmetric cerebral lesions following encephalitis.

Global amnesia after herpes simplex encephalitis has been typically associated with lesions of anterior and medial temporal lobe, inferior and medial frontal lobe, and insula. The neuropathologic correlates of this disease are usually considered to be bilateral and similar across cases. We describe a 27-year-old woman whose chronic amnesia and cerebral lesions after viral encephalitis indicate a different pattern. Two features distinguish her presentation: (1) markedly asymmetric lesions extensively involving the right temporal lobe but sparing almost all of the same structures on the left and (2) severe compromise of nonverbal learning and a nonverbal retrograde amnesia in contrast to disproportionately small impairments of verbal learning and retention. The findings suggest that encephalitis patients cannot be treated as a homogeneous group and that detailed analysis of variability in their anatomic lesions may be an important explanatory factor in neural accounts of these severe human amnesias.

Adolescent↗

PubMed1996

Fatal Sindbis virus infection of neonatal mice in the absence of encephalitis.

A comparative pathogenesis study was performed in neonatal mice using a molecularly cloned laboratory variant of Sindbis strain AR339, designated TRSB, and a single-site attenuated mutant of TRSB derived by site-directed mutagenesis of the E2 glycoprotein from Ser to Arg at residue 114 (TRSBr114). TRSB caused 100% mortality with an average survival time of 3.0 +/- 0.7 days, whereas mice inoculated with TRSBr114 exhibited an attenuated disease course with 46% mortality and an extended average survival time of 7.5 +/- 3.4 days for those animals that died. Reduced virulence of TRSBr114 was characterized by delayed appearance of detectable virus, relative to TRSB, and by lower peak virus titers in both sera and brains of infected mice. TRSB infection induced very high peak serum titers of interferon alpha/beta (215,000 units/ml compared to 2100 units/ml for TRSBr114). In situ hybridization analysis demonstrated replication of TRSB in brain, but only minimal histopathological changes and no evidence of encephalitis were observed. However, extensive extraneural lesions and viral replication were found in skin, connective tissue, and muscle. Moreover, dramatic involution of the thymus and loss of hematopoietic tissues were observed in the absence of virus replication at these sites, suggesting the involvement of a systemic physiological stress response in TRSB infection. TRSBr114 infection did not cause thymic lesions. Otherwise, the attenuated mutant demonstrated a similar pattern of tissue and organ involvement, but lesions and positive in situ hybridization signal were much more limited in scope and intensity compared to TRSB. TRSBr114-infected mice developed myositis and encephalomyelitis approximately 6 days postinfection. Therefore, TRSB-infected animals may succumb to an early syndrome associated with the stress response, preventing their survival for a time sufficient for the development of encephalitis. Alternatively, a systemic stress response, as evidenced by thymic involution, may result in immunosuppression, thus contributing to the absence of encephalitis. In any event, the attenuating mutation in the E2 glycoprotein significantly altered the course of Sindbis-induced disease by limiting virus replication and associated damage early in infection. Mutant-infected animals survived beyond Day 4 and progressed to a classical encephalomyelitis from which about half recovered.

3T3 Cells↗

PubMed1996

Genetic characterization of two phenotypically distinct North American ovine lentiviruses and their possible origin from caprine arthritis-encephalitis virus.

Ovine and caprine lentiviruses are closely related genetically and antigenically although the diseases that these viruses cause in their respective host animals can vary greatly. In sheep, syndromes consist primarily of interstitial pneumonia with rare occurrences of arthritis and encephalitis, whereas in goats, the disease expresses mainly as arthritis in adult animals with rare cases of encephalitis in newborns. Experimentally, viruses from either sheep or goats can infect animals of the reciprocal species and many field strains of ovine lentivirus have biological properties similar to those of caprine viruses. However, a molecular correlation for the phenotypic differences between ovine and caprine lentivirus strains is unknown. To investigate this, we examined genetic characteristics of two phenotypically distinct North American ovine lentiviruses. Nucleotide sequence analysis of the envelope regions from virus strains 85/34 and 84/28 showed that despite significant biological differences, these viruses are closely related to each other and are genotypically more homologous to caprine arthritis-encephalitis virus (CAEV) than to visna virus of sheep. Furthermore, analysis of the nucleotide substitutions in their env regions indicated that when differences between the two ovine viruses and CAEV were found, the changes often resulted in nucleotides homologous with visna virus. These results suggest that the two field strains of ovine lentivirus may have originated from a cross-species infection of sheep by a CAEV-like virus and, evolution of their genomes toward that of ovine lentivirus may be reflective of adaptation of these viruses to the new ovine host.

Animals↗

PubMed1999

Role of nitric oxide in pathogenesis of herpes simplex virus encephalitis in rats.

The role of nitric oxide (NO) in the pathogenesis of viral encephalitis was investigated by using an experimental model of herpes simplex virus type 1 (HSV-1) encephalitis in Lewis rats. The expression of inducible NO synthase (iNOS) mRNA determined by Northern blotting was observed first in the olfactory bulb and the brain stem on day 5 after intranasal inoculation of HSV-1, and thereafter iNOS mRNA was detected in other brain regions, i.e., cerebrum and cerebellum. In various parts of the brain, excessive NO production was identified by electron spin resonance spectroscopy. The temporal and spatial patterns of iNOS expression coincided with those of viral propagation, as demonstrated by polymerase chain reaction for HSV-1 gene expression as well as by the plaque-forming assay. Immunohistochemical study determined that iNOS was localized mainly in monocyte-derived macrophages. Treatment of virus-infected animals with the NOS inhibitor Nomega-monomethyl-l-arginine (l-NMMA), but not Nomega-monomethyl-d-arginine, significantly ameliorated not only clinical symptoms such as paralysis and seizures but also mortality. Virus yield from brain tissue was not affected by l-NMMA treatment. It is of interest that increased expression of the antioxidant enzyme heme oxygenase-1 was observed in the HSV-1-infected brain; this increased expression was strongly inhibited by l-NMMA treatment. These data suggest that the high level of NO produced by iNOS is a pathogenic factor in HSV-1-induced encephalitis in rats.

Animals↗

PubMed2004

Semliki forest virus infection of laboratory mice: a model to study the pathogenesis of viral encephalitis.

Semliki Forest virus (SFV) infection of the laboratory mouse provides an experimental system to study the pathogenesis of viral encephalitis. Following extraneural inoculation the virus is efficiently neuroinvasive and crosses the blood-brain barrier to initiate perivascular foci of infection in neurons and oligodendrocytes. The outcome of infection ranges from clinically unapparent mild encephalitis to fatal panencephalitis. SFV infections of the developing nervous system are always highly destructive and are generally fatal. In contrast, SFV infections of the mature nervous system can result in persistent infection with no apparent cell loss. This dramatic difference is attributable to developmental changes in the interactions between virus and CNS cells. Antibody responses clear the systemic infection and control the CNS infection. CD8+ T-cells are required to generate the lesions of inflammatory demyelination which can be a feature of the neuropathology. This article reviews the pathogenesis of SFV encephalitis, describing the neuropathology and the mechanisms which underlie it and which may be fundamental to many viral encephalitides.

Alphavirus Infections↗

PubMed1994

Age-dependent susceptibility to fatal encephalitis: alphavirus infection of neurons.

Sindbis virus encephalitis in mice provides a model for studying age-dependent susceptibility to acute viral encephalitis. The AR339 strain of SV causes fatal encephalitis in newborn mice, but weanling mice recover uneventfully. Increased virulence for older mice is associated with a single amino acid change from Gln to His at position 55 of the E2 glycoprotein. Weanling mice with normal immune systems clear infectious virus from neurons through an antibody-mediated mechanism. This does not happen in newborn mice because the infected neurons die soon after they are infected. Death in immature neurons, as well as most other mammalian cells infected with Sindbis virus, occurs by induction of apoptosis. This can be prevented by cellular expression of bcl-2, an inhibitor of apoptosis, which is expressed by mature neurons in culture. We conclude that mature neurons are resistant to induction of apoptosis after infection with SV through expression of cellular inhibitors of apoptosis. This provides the opportunity for antibody to clear virus by a noncytolytic mechanism.

Aging↗

PubMed1990

Evolution of post-natal herpes simplex virus encephalitis to multicystic encephalopathy.

A 3-week-old, previously healthy infant developed biopsy-proven Herpes virus type 2 (HSV-2) encephalitis. The encephalitis was characterized by cells having intranuclear inclusions and was without evidence of inflammation or hemorrhage. Neuroimaging studies did not show any destructive lesions in the brain. In spite of antiviral therapy, the infant's neurological conditions deteriorated, and the patient died at the age of 18 weeks. Post-mortem examination showed that most of the cerebral hemispheres were replaced by multiloculated cystic cavities of various sizes, typical of multicystic encephalopathy (MCE). The cystic lesions were randomly distributed and were not confined to any vascular territory. By light microscopy, there were no features of viral infection in the brain. Although in situ hybridization of the biopsy specimen taken during the acute phase of the disease demonstrated abundant HSV genome, this same method failed to detect HSV on the post-mortem specimen. These findings suggest that HSV-2 can induce MCE. Furthermore, the absence of histological features of viral encephalitis and the failure to demonstrate viral genome in the brain at autopsy does not exclude an infectious etiology in certain cases of MCE.

Autopsy↗

PubMed1990

Coxsackie B antigen in the central nervous system of a patient with fatal acute encephalitis: immunohistochemical studies of formalin-fixed paraffin-embedded tissue.

A case of fatal acute encephalitis due to Coxsackie B1 virus is described. Confirmation of Coxsackie B virus as the etiological agent of encephalitis was based on identification of the virus antigen in formalin-fixed paraffin-embedded tissue sections. In the past, the diagnosis was obtained by serological studies of peripheral blood and viral isolation. This is the first report in which indirect immunofluorescent and immunoperoxidase methods using rabbit antiserum raised against Coxsackie B types 1-6 was utilized in determining the etiology of encephalitis. It must be emphasized that these methods can be used both on biopsy or autopsy specimens, even retrospectively.

Antigens, Viral↗

PubMed1975

Transient enlargement of deep medullary veins in encephalitis.

This case report concerns a woman who presented an atypical clinical pattern with some features of encephalitis and other features of brain tumor. Cerebral angiography showed a unilateral cerebral mass with prominence of deep medullary veins, usually interpreted as evidence of a neoplasm. Brain biopsy was interpreted as astrocytoma. Subsequent spontaneous clinical remission and regression of angiographic findings led to a reappraisal of the microscopic interpretation with a final diagnosis of encephalitis. The pathogenesis of cerebral angiographic abnormalities observed with encephalitis is reviewed. The transient prominence of deep medullary veins is probably due to hyperemia. Followup angiography is recommended when encaphalitis is suspected.

Adult↗

PubMed1996

MRI of encephalitis in children: comparison of CT and MRI in the acute stage with long-term follow-up.

We examined 14 children aged 28 days to 12.7 years with encephalitis by CT or MRI. Of the patients examined by CT 58% had a normal first scan, whereas all MRI investigations demonstrated abnormalities. The clinical features correlated with several MRI investigations. On MRI herpes (HSV) encephalitis started in the medial temporal lobe and encephalomalacia developed within a few weeks. All patients had a follow-up examination 0.5 to 6.5 years after the acute phase. MRI revealed abnormalities in 13 of the 14 children; one boy, with lesions in only the white matter, had a normal follow-up MRI. Even with immediate, optimal therapy the children demonstrated severe parenchymal abnormalities. Signal abnormalities seen in the acute phase of the disease were likely to persist. In children with HSV encephalitis atypical lesions in different areas were seen.

Acute Disease↗

PubMed1988

Herpes-simplex-related antigen in human demyelinative disease and encephalitis.

Using immunohistochemical methods optimized to detect herpes simplex virus type 2 (HSV-2) antigen, paraffin sections from human central nervous system tissues from 31 cases pathologically diagnosed as multiple sclerosis (MS), 34 cases of other neurological diseases, 4 adult cases of HSV encephalitis, and mouse brains infected with various HSV strains were examined. Two distinct patterns of immunoreactivity with HSV antisera were seen. In typical acute human and experimental encephalitis, antigen was readily detected using high dilutions of antisera to both HSV types -1 and -2, and was found nonselectively in both neurons and glia. Lesions were destructive, with necrosis of all neural cell types, and inflammation was a mixture of polymorphonuclear and mononuclear cells. By contrast, immunoreactivity in lesions in each of three MS cases and in one case of brain stem encephalitis was found only with HSV-2 antisera, and relatively high antiserum concentrations were required to detect it. Reactivity appeared to be largely restricted to glial cell nuclei within and near lesions that were selectively demyelinated. Only mononuclear inflammation was present. These experiments suggest that HSV-related antigen may be found in a broader spectrum of human CNS lesions than has previously been recognized, and that HSV or a related agent may be associated with a selective infection of glial cells and with CNS demyelination.

Adult↗

PubMed1988

Microglia in the giant cell encephalitis of acquired immune deficiency syndrome: proliferation, infection and fusion.

The autopsied brains of three homosexual men with acquired immune deficiency syndrome (AIDS), progressive encephalopathy and widespread multinucleated giant cell encephalitis were investigated by lectin and immunohistochemical methods to ascertain the cellular distribution of a human immunodeficiency virus (HIV) core protein, p25. Abundant viral antigen was present in all brains, limited to perivascular macrophages, microglial and multinucleated cells, some bearing elongated cytoplasmic processes. The multinucleated cells were consistently labelled by the lectin Ricinus communis agglutinin-1, a marker for microglia, which demonstrated process-bearing variants of these cells. The prominent staining of microglia for viral antigen and the morphological suggestion that they fuse with other microglia and/or macrophages to form the multinucleated cells characteristic of HIV encephalitis indicate that microglia are probably direct targets of HIV infection and serve to propagate and amplify this retroviral encephalitis.

Acquired Immunodeficiency Syndrome↗

PubMed1980

Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living ameba.

Primary amebic meningoencephalitis and granulomatous amebic encephalitis are well recognized clinicopathological entities caused by free-living amebas. Associated arteritis and "mycotic aneurysms" with infiltration of intracranial arteries by lymphocytes, amebic trophozoites and cysts have not been previously reported. A 26-month-old girl had a 3-week history of encephalitis, characterized, initially, by vomiting and low-grade fever. Subsequently, she developed ataxia, generalized weakness, lethargy, and esotropia. The first CSF showed 490 RBC/microliters, 705 WBC/microliters with 90% mononuclears. Her pupils reacted briskly to light. Moderate nuchal rigidity, nystagmus, fixed downward gaze, anisocoria, bilateral 6th nerve palsy, left arm monoparesis and left Babinski were present. CAT scan revealed slight symmetrical dilatation of anterior horns of lateral ventricles and an area of abnormal enhancement above the 3rd ventricle. She died 14 days after admission, 5 weeks after onset of symptoms. The brain showed focal necrotizing encephalopathy, involving thalami, cerebellum, brain stem, and cervical and upper thoracic spinal cord. Numerous free-living amebic trophozoites and cysts were present within a chronic granulomatous encephalitis. There were trombosis of basilar, posterior cerebral, and vertebral arteries with profuse chronic panarteritis, fibrinoid necrosis, and mycotic aneurysms.

Amebiasis↗