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At least 19 recordsLinked to original sources
PubMed1997

[Viral encephalitis].

Viral infections of the nervous system make up a wide range of disorders with a mainly benign outcome. However, in some cases there is severe, morbimortality. In viral encephalitis there is direct involvement of the brain parenchyma which is seen clinically as reduced consciousness, convulsions and/or focal neurological deficit. The especial attraction of some viruses for particular cells or structures determines the variety of clinical findings. The incidence and frequency of the various agents depends on several factors (geographical location of a certain virus, age and general health of the population concerned, etc.). In areas free of arbovirus the commonest aetiologies are; varicella, herpes simplex, parotiditis and enterovirus. Modern treatment (transplants, chemotherapy) of previously fatal diseases and the AIDS epidemic have increased the number of immunodeficient patients; the population is susceptible to viral infections of the nervous system which are infrequent (e.g. cytomegalovirus, papovavirus) or which follow a different course (e.g. measles, enteroviruses) to that in immunocompetent patients. Specific conditions are reviewed. Improvement in the general health and sanitation of the population, and the universal use and development of new vaccines will significantly reduce the incidence of viral encephalitis. Improved prognosis will be related to the use of modern laboratory techniques which permit early, sensitive, specific diagnosis and the development of antiviral agents.

Adenoviridae↗
PubMed2004

Differential regulation of innate and adaptive immune responses in viral encephalitis.

Viral encephalitis is a global health concern. The ability of a virus to modulate the immune response can have a pivotal effect on the course of disease and the fate of the infected host. In this study, we sought to understand the immunological basis for the fatal encephalitis following infection with the murine coronavirus, mouse hepatitis virus (MHV)-JHM, in contrast with the more attenuated MHV-A59. Distinct glial cell cytokine and chemokine response patterns were observed within 3 days after infection, became progressively more polarized during the course of infection and with the infiltration of leukocytes. In the brain, MHV-JHM infection induced strong accumulation of IFNbeta mRNA relative to IFNgamma mRNA. This trend was reversed in MHV-A59 infection and was accompanied by increased CD8 T cell infiltration into brain compared to MHV-JHM infection. Increased apoptosis appeared to contribute to the diminished presence of CD8 T cells in MHV-JHM-infected brain with the consequence of a lower potential for IFNgamma production and antiviral activity. MHV-JHM infection also induced sustained mRNA accumulation of the innate immune response products interleukin (IL)-6 and IL-1. Furthermore, high levels of macrophage-inflammatory protein (MIP)-1alpha, MIP-1beta, and MIP-2 mRNA were observed at the onset of MHV-JHM infection and correlated with a marked elevation in the number of macrophages in the brain on day 7 compared to MHV-A59 infection. These observations indicate that differences in the severity of viral encephalitis may reflect the differential ability of viruses to stimulate innate immune responses within the CNS and subsequently the character of infiltrating leukocyte populations.

Animals↗
PubMed1999

[Viral encephalitis].

Viral encephalitis presents with fever, headache, focal and generalized neurologic symptoms and signs, seizures, and CSF pleocytosis. Herpes simplex Virus (HSV) 1 and arboviruses (flaviruses) are the most common causes of encephalitis in Switzerland. The initial work-up in a suspected encephalitis includes CSF analysis, EEG, and brain CT or MRI. The identification of the responsible agent usually occurs with polymerase chain reaction or serology. The differential diagnosis to other infectious and non-infectious acute CNS-disorders may initially be arduous. A specific treatment is possible only in encephalitis caused by viruses of the herpes group. Active immunization should be considered in subjects at high risk for tick-borne encephalitis. With early treatment the prognosis may be satisfactory also in HSV encephalitis.

Antiviral Agents↗
PubMed1992

Cerebral oxygen extraction during severe viral encephalitis.

Viral encephalitis can cause devastating neurologic injury. Little is known about cerebral hemodynamics and metabolism in this condition. We report two patients with severe encephalitis, one proven and the other suspected to be due to herpes simplex, in whom the global cerebral oxygen extraction ratio (OER) and carbon dioxide (CO2) responsiveness was assessed. OER was low in both patients throughout the acute period. CO2 responsiveness was present initially in both and disappeared later in the more severely affected child. These cases demonstrate that cerebral hyperemia occurs in severe viral encephalitis and that hyperventilation can effectively reduce the intracranial pressure.

Blood Gas Analysis↗
PubMed1993

Viral encephalitis.

Viral encephalitis represents an important source of morbidity and mortality worldwide. Numerous viruses possess neurovirulence, producing encephalitic disorders that usually consist of fever, headache, vomiting, altered consciousness, focal or generalized seizures, and motor dysfunction. Contemporary virologic methods frequently allow rapid and specific identification of viral pathogens, but the etiologic agent remains uncertain in 25% or more of encephalitis patients. Although acyclovir substantially reduces mortality and improves outcome for patients with herpes simplex virus encephalitis, supportive care remains the only therapy available for most patients with virus encephalitis.

Antiviral Agents↗
PubMed2001

LaCrosse viral encephalitis mimics herpes simplex viral encephalitis.

Temporal lobe abnormalities, findings commonly associated with herpes simplex virus encephalitis, were observed in a male 10 years of age found to have LaCrosse virus encephalitis. Diagnostic features included magnetic resonance imaging revealing abnormal signal intensity in the bilateral frontotemporal regions, and left-sided periodic lateralizing epileptiform discharges. LaCrosse virus encephalitis should be included in the differential diagnosis of viral encephalitis associated with structural and electrographic temporal lobe lesions, represented by periodic lateralizing epileptiform discharges. The recently developed LaCrosse RNA polymerase chain reaction for cerebrospinal fluid may enable rapid diagnosis, prevent the need for treatment with acyclovir, and give parents an encouraging prognosis.

Child↗
PubMed2005

Viral encephalitis.

Acute viral encephalitis may be caused by a wide range of viruses but the most important is herpes simplex encephalitis (HSE) because of its severity, especially if untreated, and its good response to specific treatment with acyclovir. The outcome of any CNS viral infection is dependent on both the immune status of the host and the virulence of the infecting virus. In evaluating a patient with suspected viral encephalitis there are 3 essential steps, namely the identification of a true parenchymal virus infection of the brain rather than a non-infective encephalopathy, the distinction of an infectious viral encephalitis from an acute disseminated encephalomyelitis (ADEM), and then the determination, where possible, of the specific virus involved. In practice, the precise viral cause of the encephalitis may never be established. Analysis of the CSF for herpes simplex virus (HSV) DNA using the Polymerase Chain Reaction (PCR) has been a significant advance in the diagnosis of HSE as this test has a very high sensitivity and specificity especially with appropriate sample timing. It is essential to commence early treatment with intravenous acyclovir in patients suspected of having HSE because of the remarkable safety and efficacy of this drug and the dangers of delaying potentially effective treatment of life threatening disease. This review outlines the general management approach in patients suspected of having viral encephalitis.

Encephalitis, Herpes Simplex↗
PubMed2004

Bichat guidelines for the clinical management of viral encephalitis and bioterrorism-related viral encephalitis.

Most of the viruses involved in causing encephalitis are arthropod-borne viruses, with the exception of arenaviruses that are rodent-borne. Even if little information is available, there are indications that, most of these encephalitis-associated viruses could be used by aerosolisation during a bioterrorist attack. Viral transfer from blood to the CNS through the olfactory tract has been suggested. Another possible route of contamination is by vector-borne transmission such as infected mosquitoes or ticks. Alphaviruses are the most likely candidates for weaponisation. The clinical course of the diseases caused by these viruses is usually not specific, but differentiation is possible by using an adequate diagnostic tool. There is no effective drug therapy for the treatment of these diseases and treatment is mainly supportive, but vaccines protecting against some of these viruses do exist.

Bioterrorism↗
PubMedDate not supplied

[Frequency of neuropsychiatric signs and symptoms in patients with viral encephalitis].

INTRODUCTION: Acute viral encephalitis (AVE) is a frequent condition that usually courses with psychiatric alterations but few systematic studies have been conducted to investigate it. AIMS: To determine the frequency and the progression of the neuropsychiatric symptoms in patients with AVE. PATIENTS AND METHODS: A retrospective study was carried out. AVE was defined as an acute and progressively coursing condition in previously healthy subjects, with clinical signs of diffuse alteration of the central nervous system, abnormal electroencephalogram and/or inflammatory cerebrospinal fluid (CSF). We excluded patients who previously had epilepsy, a positive serodiagnosis for human immunodeficiency virus (HIV), and cases compatible with herpes simplex encephalitis from electroencephalographic or imaging data with focalisation towards temporal, frontal, regions or a positive DNA test for herpes in CSF. Finally, 83 patients were included. The psychiatric signs and symptoms that were produced were recorded during the acute phase and one year after discharge from hospital (sequelae). RESULTS: The psychiatric disorders in the acute phase were psychomotor agitation (67%), drowsiness (55%), disorientation (47%), visual hallucinations (43%) and aggressiveness (34%). One year after hospitalisation, in a sample of 70 patients in a clinical control, we found memory disorders (16%), aggressiveness (9%), aphasia (8%), visual hallucinations (8%), and auditory hallucinations (7%). The mortality rate was 6%. CONCLUSIONS: Neuropsychiatric disorders are very frequent during the acute phase of viral encephalitis, which is relevant for the differential diagnosis in patients who visit emergency departments with behavioural disorders. One year after hospital discharge, the main sequelae are of a neuropsychiatric nature and cognitive impairment is predominant.

Adolescent↗
PubMed2003

Geographic dynamics of viral encephalitis in Thailand.

Viral encephalitis (VE) continues to be a major disease in Asia, causing serious illness which may result in death or have neurological sequelae. This study involves an ecological analysis of the climatic, geographic and seasonal patterns of clinically reported VE in Thailand from 1993 to 1998 to investigate regional and seasonal differences in disease incidence. Three thousand eight hundred and twenty nine cases of VE were clinically diagnosed nationwide during the study period by the Thai Ministry of Public Health. Spearman rank correlations of temporal, spatial and geographic variables with disease incidence were performed. The monthly incidence of VE correlated significantly with seasonal changes in temperature, relative humidity and rainfall in the north-northeast region of Thailand (P < 0.001), whereas incidence in the south-central region correlated only with relative humidity (P = 0.003). Spatial analysis revealed a positive correlation of disease with elevation (P < 0.001), and negative correlations with rice-field cover (P < 0.001), agricultural land-use (P < 0.001) and temperature (P = 0.004) in the north-northeast region. No significant spatial correlation was identified in the south-central region. The spatial distribution of VE suggests that etiologic variations may be responsible, in part, for the geographic patterns of disease. Active etiologic surveillance is necessary in a variety of geographic settings in order to provide physicians with information necessary for disease prevention and clinical management.

Age Distribution↗
PubMed1997

[Radiological diagnosis of viral encephalitis].

Most of viral encephalitis may demonstrate no specific change on CT and MR images. Brain swelling, edema, abnormal density (CT) and abnormal intensity (MR) can be detected in herpes simplex encephalitis and enterovirus encephalitis (coxsackie, echo, polio). The common finding on CT and MRI in patients with HIV encephalopathy are atrophy, leukomalacia. Progressive multifocal leukoencephalopathy (PML) shows multifocal oval or round white matter T2-hyperintensities on MR images. Subacute sclerosing panencephalitis (SSPE) may present slight changes in the subcortical and periventricular white matter, as well as basal ganglia. Progressive disorder makes widespread T1-low, T2-high intensity area and atrophy. MRI of acute disseminated encephalomyelitis (ADEM) shows multifocal subcortical hyper intense foci on T2-weighted studies. The deep white matter, brainstem, thalamus and cerebellum can be affected. Most of ADEM lesions resolve. Imaging findings of acute lymphocytic meningitis by echovirus and coxsackievirus are usually normal.

Encephalitis, Viral↗
PubMed2005

History of U.S. military contributions to the study of viral encephalitis.

The viral encephalitides represent 15% (9 of 62) of the infectious diseases identified by the Armed Forces Medical Intelligence Center as being of U.S. military operational importance. Japanese encephalitis, tick-borne encephalitis, Venezuelan equine encephalitis, Eastern equine encephalitis, Western equine encephalitis, West Nile fever, rabies, St. Louis encephalitis, and Murray Valley (Australian) encephalitis are included on the Armed Forces Medical Intelligence Center threat list. This article reviews the U.S. military contributions to the prevention and control of the first seven of these.

Biomedical Research↗
PubMed2005

Paraneoplastic limbic encephalitis presenting as acute viral encephalitis.

OBJECTIVE: To describe a case of limbic encephalitis which initially presented as viral limbic encephalitis and during the clinical evaluation a renal carcinoma was diagnosed. CASE REPORT: Patient with history of peripheral paresis of right facial nerve, 1 month after symptoms appearance and treatment, developed fever, vomiting, grand mal seizure, decreased level of consciousness, confusion, hallucinations and agitation. The patient initially presented a clinical picture of viral LE. which confirmed by CSF. MRI brain showed areas with pathological intensity signal in the region of limbic system unilateral. During the clinical evaluation a renal carcinoma was discovered and a nephrectomy has been performed. CONCLUSIONS: Although PLE typically presents as a chronic or subacute disease, it may be fulminant and clinically indistinguishable from an acute HSVE. This association pose the problem of a possible relation between this two syndromes and the correct diagnosis is very important, because there are effective treatments.

Acute Disease↗
PubMed1983

Pathogenesis of viral encephalitis: demonstration of viral antigen(s) in the brain endothelium.

One of the enigmas in the pathogenesis of inflammation is why the white cells adhere to the endothelium. In trying to define the pathogenic mechanism, we carried out experiments on ferrets infected with an SSPE strain of measles virus. Using immunoperoxidase labeling techniques, viral antigens were demonstrated on the luminal surface and in the cytoplasm of endothelial cells, irrespective of the presence or absence of inflammatory changes. The degree of inflammation corresponded well with antibody titer. These data suggest that the viral antigen in the endothelial cells is the site of interaction between these cells and sensitized lymphoid cells.

Animals↗
PubMed1989

[Viral encephalitis].

Acute viral and other infectious causes of encephalitis usually produce fever, headache, stiff neck and alterations in consciousness, focal neurologic signs and seizures. A large number of viral and nonviral agents can cause encephalitis. Arthropod-borne viruses peak in summer, the tick-borne infections occur in early summer, enterovirus infections in later summer and mumps in the winter and spring.

Acyclovir↗
PubMed2002

Subcortical low intensity on MR images of meningitis, viral encephalitis, and leptomeningeal metastasis.

BACKGROUND AND PURPOSE: Subcortical low-intensity lesion on T2-weighted images is an uncommon manifestation of ischemia, multiple sclerosis, and Sturge-Weber disease. This study was performed to determine whether subcortical low signal intensity is an MR feature of meningitis, viral encephalitis, or leptomeningeal metastasis and to investigate a cause of subcortical low intensity. METHODS: We retrospectively reviewed MR images of 117 patients with meningitis, encephalitis (viral or unknown), or leptomeningeal metastasis for the presence of subcortical low intensity, meningeal enhancement, signal intensity change of cortex, and change in subcortical low intensity on follow-up images. Diffusion-weighted (DW) images and apparent diffusion coefficient (ADC) maps were obtained in 55 patients. Subcortical low-intensity lesions were also quantitatively analyzed on T2-weighted, fluid-attenuated inversion recovery (FLAIR), and DW images. RESULTS: Subcortical low intensity was found in nine (23.7%) of 38 patients with encephalitis (viral, 31; unknown origin, 7), five (24%) of 21 with leptomeningeal metastasis, and five (9%) of 58 with meningitis. Leptomeningeal enhancement was observed in 100% and cortical hyperintensity in 14 (74%) of 19 patients with subcortical low intensity. Leptomeningeal enhancement was seen in 46 (47%) and cortical hyperintensity in 33 (34%) of 98 patients without subcortical low intensity. Subcortical low intensity disappeared or decreased in extent on follow-up MR images in all seven patients who underwent follow-up. ADC of subcortical low-intensity lesions was lower than that of the contralateral area and decreased by 9.3 +/- 11.4%. CONCLUSION: Subcortical low intensity was uncommonly found in meningitis, viral encephalitis, and leptomeningeal metastasis. It is a nonspecific MR sign of various meningeal and cortical diseases. Although the cause of subcortical low intensity remains uncertain, free radical formation may play a role as a causative factor.

Adolescent↗