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PubMed2006

Polymorphisms of the gene coding for copper/zinc superoxide dismutase (SOD1) in patients with Japanese encephalitis.

Japanese encephalitis is the commonest form of encephalitis globally. Most cases develop characteristic encephalitis but some also present with flaccid paralysis. The paralysis is secondary to damage at the alpha motor neurone, the site that is also damaged in amyotrophic lateral sclerosis (ALS). The gene coding for superoxide dismutase 1 (SOD1) is thought to be involved in ALS and may also be linked to susceptibility to Japanese encephalitis. To investigate this possibility, polymorphisms in the SOD1 gene were investigated, in 61 cases of Japanese encephalitis, 61 matched controls and 171 population controls, in Vietnam. Novel polymorphisms, found only in three of the cases and one of the population controls, may be involved with susceptibility to Japanese encephalitis and potentially to other flavivirus infections that lead to damage to the cells of the anterior horn. Further research on this possible association is required.

Adolescent↗
PubMed2004

Epidemic encephalitis and American neurology, 1919-1940.

Encephalitis lethargica, also known as epidemic encephalitis, emerged as a new infectious disease near the end of the First World War. Bacteriologic, epidemiologic, and clinical investigation produced no clear consensus regarding the nature of the disease, even as several other experimentally demonstrable "encephalitides" appeared on the scene. By 1940, new encephalitis lethargica cases had almost entirely disappeared, and neurologists renamed this once-novel infection as an amorphous syndrome of marginal interest. A variety of forces influencing the fate of encephalitis lethargica's epidemic status can be seen at work in the Matheson Commission, whose members hoped to use encephalitis as a model disease that might supplant their reliance on clinical phenomenology with a causal analysis of nervous disease grounded in the laboratory. When it failed to live up to these expectations, the model was abandoned. Epidemic encephalitis was soon forgotten.

Encephalitis, Arbovirus↗
PubMed2006

Long-term cognitive and motor deficits after enterovirus 71 brainstem encephalitis in children.

OBJECTIVES: Several large outbreaks of enterovirus 71 infections have occurred in Taiwan during the past decade. Brainstem encephalitis was the most common neurologic complication. This study was designed to determine the long-term cognitive and motor outcomes of children with enterovirus 71 brainstem encephalitis. METHODS: We conducted a prospective follow-up study of children who met the case definition for enterovirus 71 brainstem encephalitis. Subjects were stratified into isolated brainstem encephalitis (stage II), autonomic nervous system dysregulation (stage IIIa), and pulmonary edema (stage IIIb). The subjects and their parents or guardians were interviewed using structured questionnaires and received comprehensive cognitive and neurologic examinations. Motor coordination, visual-motor skill, and intellectual ability were evaluated. RESULTS: Follow-up studies were conducted in 63 previously healthy children with enterovirus 71 brainstem encephalitis (49 stage II, 7 stage IIIa, and 7 stage IIIb). The mean time to follow-up was 2.8 +/- 1.0 years (range: 1.4-4.9 years). Boys outnumbered girls by 3 to 2. The mean age at diagnosis was 2.4 +/- 1.4 years (range: 0.3-7.1 years). The most common abnormal neurologic findings on admission were altered consciousness (47.6%), followed by abnormal activities of daily living (52.4%), cerebellar dysfunction (17.5%), and cranial nerve palsy (15.9%). At follow-up, 51 of 63 children had no detectable deficits. Among the remaining 12 children, 3 died during the follow-up. The remaining 9 children (14.3%) had residual deficits. Two of these with stage IIIb disease continued to have severe motor and respiratory failure. CONCLUSIONS: Residual defects were still present in a significant proportion of children with enterovirus 71 brainstem encephalitis at >2 years after their hospitalization. Children with stage II disease were most likely to have residual cerebellar defects. Those with stage IIIb disease continued to have severe respiratory and motor impairment. Long-term follow-up of this cohort is needed to determine the ultimate prognosis.

Brain Stem↗
PubMed2002

Acute viral encephalitis: the recent progress.

In the new Japanese control law for infectious diseases, most varieties of acute viral encephalitis belong to Category IV requiring report of all cases at sentinel hospitals. Herpes simplex virus type 1 (HSV-1) encephalitis comprises the majority of cases. With the increased prevalence of diagnostic procedures such as polymerase chain reaction (PCR), several forms of HSV-1, and -2 central nervous system (CNS) infections, including acute disseminated encephalomyelitis, brainstem encephalitis, and myelitis, have been clarified. Since 1990 we have conducted a survey of HSV CNS infections in the Kyushu and Okinawa regions, and the data are reviewed here. Trends include an increase in a new subtype of non-herpetic acute limbic encephalitis. In contrast, the incidence of Japanese encephalitis (JE) in Japan has dramatically decreased to a few patients per year; however, JE remains a threat for those with decreased or absent immunity to the JE virus. Imported emerging and reemerging CNS infections such as Murray Valley and West Nile encephalitis can occur in Japan. Influenza-associated encephalitis/encephalopathy is also described as a threat for adults as well as young children.

Acute Disease↗
PubMed1998

Epizootiology, pathology, and ultrastructure of the myxosporean associated with parasitic encephalitis of farmed Atlantic salmon Salmo salar in Ireland.

In 1995 at a sea-farm in Ireland, Atlantic salmon Salmo salar smolts were introduced in the spring and autumn into 2 marine rearing sites, one with and one without recent histories of neurologic disease and mass mortality believed to be due to parasitic encephalitis. In order to monitor disease, determine the onset and anatomic distribution of parasites and encephalitis, and determine the ultrastructure and identity of the parasite, randomly selected smolts were necropsied from both sites at intervals of 1 to 3 d for periods of 1 to 2 mo, and clinical signs and cumulative mortalities were monitored. The prevalences of parasites and encephalitis were assessed by light microscopy, and sections of brain were examined by transmission electron microscopy. No clinical signs of neurologic disease were observed, but parasites and encephalitis were detected in smolts from both sites, with prevalences of each that were significantly greater in smolts from the site with recent disease. Based on light microscopy, the parasite was first detected in smolts sampled at 26 d post-introduction. Parasites were detected with significantly greater frequency in the optic tectum of the mesencephalon than in the diencephalon, metencephalon, and myelencephalon, and were not detected in the telencephalon. Foci of non-suppurative encephalitis were detected with significantly greater frequency in the myelencephalon than in each of the other 4 anatomic subdivisions. In each anatomic subdivision the prevalence of encephalitis was significantly greater than that of parasitic infection. The ultrastructure of the parasite was consistent with that of a histozoic presporogonic multicellular developmental stage of a myxosporean, characterized by intercellular branching tubular structures containing generative cells arranged individually or in cell-in-cell doublets. Parasitic stages were located between bundles of axons, with compression of axons along segments of their plasmalemma. No mature spores were detected.

Animals↗
PubMed1988

Ecological studies of Japanese encephalitis virus in Hokkaido: interepidemic outbreaks of swine abortion and evidence for the virus to overwinter locally.

Outbreaks of abortion and stillbirth caused by Japanese encephalitis virus were observed in swine populations in Hokkaido in 1984 and 1985. Two strains of Japanese encephalitis virus were isolated from aborted fetuses in different outbreaks, and the antigenic types of the strains found to be different from Nakayama and JaGAr-01. The outbreak of 1985 was in early June, the interepidemic period of Japanese encephalitis in northern temperate zones. A seroepidemiological survey carried out from 1984 to 1986 in 14 districts showed high rates of Japanese encephalitis antibody in swine sera in two districts. A more detailed 3-year survey showed that pig farms positive for Japanese encephalitis antibody were detected at the same sites in Hiroshima near Sapporo as negative farms. These data suggest that Japanese encephalitis virus is maintained in a distinct endemic focus and has the capacity to overwinter locally in Hokkaido.

Abortion, Veterinary↗
PubMed1988

Intrathecal production of antibodies against Toxoplasma gondii in patients with toxoplasmic encephalitis and the acquired immunodeficiency syndrome (AIDS).

We attempted to determine whether patients with the acquired immunodeficiency syndrome (AIDS) and toxoplasmic encephalitis produce Toxoplasma antibodies in the central nervous system, and whether these antibodies would be useful for diagnosing toxoplasmic encephalitis. Thirty-seven patients with AIDS and toxoplasmic encephalitis and 11 patients with AIDS alone were studied. All patients had serum IgG but not IgM Toxoplasma antibodies. Twenty-three of the patients with AIDS and toxoplasmic encephalitis had Toxoplasma antibody in cerebrospinal fluid compared to none of the patients with AIDS alone. Of the patients with AIDS alone who had serum antibodies to T. gondii, none had Toxoplasma antibodies in cerebrospinal fluid. Production of antibodies in the central nervous system was seen in 11 of 16 patients with AIDS and toxoplasmic encephalitis but not in 4 patients in the control group who only had Toxoplasma antibody in their cerebrospinal fluid. These results suggest that production of T. gondii antibodies in the central nervous system may be diagnostic of toxoplasmic encephalitis.

Acquired Immunodeficiency Syndrome↗
PubMed2000

[Brain thermo-pooling is the major problem in pediatric influenza encephalitis].

The prognosis of pediatric encephalitides, such as infantile influenza encephalitis, is still poor because of the rapid progression, severe brain edema, selective bilateral basal ganglia necrosis, and a poor immune function, the mechanism of which is still unknown. Especially, little is known about virus es in CSF and brain tissue with influenza encephalitis, which hampers successful treatment of this condition. Recently, hypothermia treatment has attracted attention as the management of infantile influenza encephalitis to prevent severe brain edema. Recent clinical studies have revealed brain thermo-pooling (elevation of brain tissue temperature) with damage of blood-brain barrier (BBB). We then studied brain injury mechanism after severe brain injuries, cerebral strokes, reperfusion after shock, and high fever with lower cerebral perfusion pressure in our ICU. The brain thermo-pooling phenomenon results from body temperature higher than 38 degrees C, systolic blood temperature lower than 90-100 mmHg, and cerebral perfusion pressure (CPP) lower than 70 mmHg that hinders washout of brain tissue temperature by cerebral blood flow. We have recorded of brain tissue temperature of 40-44 degrees C in various brain injured patients. Some pathophysiological changes in infantile influenza encephalitis may be explained on the basis of this brain thermo-pooling phenomenon. In systemic infection, it causes severe brain edema by activation of cytokines and destruction of BBB, bilateral basal ganglia necrosis by acute severe brain hypoxia, resulting in poor prognosis without control of brain temperature. In other words, brain thermo-pooling, is the major target of treatment for infantile influenza encephalitis. In this paper, new concepts of the brain injury mechanism and methods of brain hypothermia treatment of pediatric influenza encephalitis are presented.

Albumins↗
PubMed1999

Herpes simplex virus-1 encephalitis in eastern Uttar Pradesh.

OBJECTIVE: To study the proportion of HSV-1 encephalitis in acute viral encephalitis. METHODS: One hundred and five patients presenting with clinical diagnosis of acute viral encephalitis and with exclusion of other possible causes of acute inflammatory brain disease prevalent in the area by relevant laboratory investigations were included in the study. Ninety single CSF samples were tested for HSV-1 IgM antibodies by ELISA test supplied by Dia Medix Corporation, USA. CT Scan and EEG studies were carried out in 25 patients. RESULTS: Clinical and neuro investigational profile of patients suggested a low incidence of HSV-1 encephalitis in the study group. IgM antibodies were present in CSF sample of one patient only. CONCLUSION: HSV-1 encephalitis constitutes a very low proportion (1.1%) of acute viral encephalitis cases seen in Eastern Uttar Pradesh (India).

Encephalitis, Herpes Simplex↗
PubMed2001

(18)F-fluorodeoxyglucose positron emission tomography and MR imaging findings in Rasmussen encephalitis.

BACKGROUND AND PURPOSE: Rasmussen encephalitis is a chronic, progressive encephalitis that manifests as an abrupt-onset, intractable seizure disorder in previously developmentally normal children. The objectives of the current study were to characterize the (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET) and MR imaging findings in Rasmussen encephalitis and to test the hypotheses that data from both imaging techniques are required to establish the diagnosis and identify the affected cerebral hemisphere in some cases. METHODS: Eleven patients with Rasmussen encephalitis were identified from a review of a computer database. The MR (n = 10) and PET (n = 11) imaging data were reviewed retrospectively and conjointly. RESULTS: On MR images, nine of 10 patients manifested bilateral cerebral atrophy that predominantly involved one hemisphere. One patient had purely unilateral cerebral atrophy. We observed foci of abnormally increased T2 signal intensity in nine of 10 patients. On FDG PET images, all patients showed extensive regions of hypometabolism within the cerebral hemisphere that showed the greatest atrophy. Discrete foci of hypermetabolism, indicative of seizure activity, were observed in six patients. The FDG PET and MR imaging findings were either stable or gradually progressive in patients with multiple imaging studies (MR, n = 5; FDG PET, n = 5). CONCLUSION: Rasmussen encephalitis is characterized by diffuse, unilateral cerebral hypometabolism on FDG PET images, with corresponding regions of cerebral atrophy on MR images. Although MR imaging data alone are sufficient to suggest a diagnosis of Rasmussen encephalitis in many cases, correlation with FDG PET data increases diagnostic confidence and allows the unequivocal identification of the affected cerebral hemisphere in patients whose MR imaging findings are subtle or distributed bilaterally.

Adolescent↗
PubMed1992

[Relation of foci of tick-borne encephalitis to original plant associations in the Czech Republic].

Based on reports of the hygiene service on the morbidity from tick-borne encephalitis during the period of 1953-1987, data in the literature and results of the authors' field research on the incidence of ticks, the authors defined foci of the disease. In Bohemia there is an extensive important focus of tick-borne encephalitis in the Central Bohemian region in the Krivoklát area, along the Berounka river, along the mid Vltava river and lower Sázava river, in the area of the Brdy mountains and Czech Karst, linked in the South along the Vltava river to foci in the South Bohemian region in the districts of Písek and Ceské Budĕjovice and in the West linked along the Berounka river with the focus in the central part of the West Bohemian region. In the North Bohemian region and East Bohemian region, only minor separate relict foci of tick-borne encephalitis were found. In Moravia there are extensive foci of tick-borne encephalitis in the North Moravian region in the districts of Opava and Bruntál, in the South Moravian region in its central and southern parts. The foci in Bohemia are separated from foci in neighbouring countries, foci in Moravia are continuous with those in Poland and Austria. It was proved that ticks and the revealed foci of tick-borne encephalitis in the Czech Republic are in areas of original oak groves. Areas of beech woods, even those which are below areas where ticks are found, i.e. lower that 700 m above sea level, do not offer favourable conditions for ticks andare not foci of tick-borne encephalitis. Assessment of areas with regard to the prevailing flora and fauna proved a useful method of prediction of the occurrence of ticks and foci of disease they transmit.

Animals↗
PubMed2003

[Decompressive craniectomy in a patient with herpetic encephalitis associated to refractory intracranial hypertension].

Herpetic encephalitis is the most common cause of viral encephalitis in our country. Pathological studies show progressive necrosis and edema in specific territories of the brain. The mortality of herpetic encephalitis was reduced from 70% to 20% with the use of intravenous aciclovir in the first three days of illness. However, almost 50% of patients develop a neurological deficit. One of the most important causes of death in herpetic encephalitis is the refractory intracranial hypertension. There are anecdotal reports of patients with refractory intracranial hypertension due to herpetic encephalitis that were treated with decompressive craniectomy with good results. We report a 21 years old female patient with herpetic encephalitis and refractory intracranial hypertension that was successfully treated with a decompressive craniectomy.

Adult↗
PubMedDate not supplied

[Limbic encephalitis: a probably under-recognized syndrome].

Limbic encephalitis was identified as a clinicopathological entity in 1968. Up to a few years ago, 200 cases were described, most associated with lung cancer and more infrequently with other tumors. The recent identification of patients with this syndrome, idiopathic limbic encephalitis, who never develop cancer and have high titers of antibodies to voltage-gated potassium channels (VGKC) and an excellent response to immunosuppressive therapy, has extended the etiological spectrum and suggests that the syndrome may be under-recognized. The disorder, which develops in a few days or weeks, is characterized by the development of short-term memory loss, seizures, confusion and psychiatric features. The presence of symptoms beyond the limbic system is highly suggestive of a paraneoplastic origin. When limbic encephalitis is suspected, the following tests should be performed in order to demonstrate: a) involvement of the temporal lobes (EEG and brain MRI); b) presence of inflammatory abnormalities in the CSF, and c) the presence of onconeural antibodies or anti-VGKC. Once the diagnosis is confirmed by the clinical picture and MRI findings, treatment must be initiated without waiting for the antibody results because its negativity does not exclude the diagnosis. Detection of an onconeural antibody will confirm that the limbic syndrome is paraneoplastic and will help us to search for an underlying tumor and to predict possible response to the treatment. The recommended treatment is cycles of methylprednisolone (1 g/day for 3 to 5 days). Therapeutic response in the idiopathic limbic encephalitis is excellent and may be good in limbic encephalitis with anti-Ma2 or without onconeural antibodies. On the contrary, immunosuppressant treatment is not usually effective in limbic encephalitis associated to anti-Hu antibodies.

Humans↗
PubMed2005

Probable chronic viral encephalitis with microglial nodules in the entire brain: a case report with necropsy.

BACKGROUND: Chronic encephalitis has rarely been seen, probably due to its viral origins, which may produce the disease in healthy or immunocompromised hosts. The etiology and pathophysiology of these types of encephalitis have not yet been clarified. CASE REPORT: A 63-year-old Japanese woman with underlying multiple myeloma developed chronic encephalitis with fever and progressive dementia, bilateral mild thalamic lesions on magnetic resonance imaging, and a prolonged pleocytosis, normal glucose value, and elevated interleukin-6 and interferon-gamma in the cerebrospinal fluid (CSF). The patient died of pneumonia 6 months after the onset of illness, and diffuse microglial nodules were found in the entire brain. No causative viral agents were identified by polymerase chain reaction and serological tests. CONCLUSIONS: The patient was presumed to have suffered from chronic viral encephalitis, based on clinical findings, including CSF and cytokine changes. Microglial nodules are observed in flavivirus group encephalitides, Rickettsia infections, and cytomegalovirus encephalitis in immunocompromised hosts. The possible pathogenesis of this rare encephalitis is discussed.

Autopsy↗
PubMed1990

To the antigenic classification of some viruses from the tick-borne encephalitis complex by monoclonal antibodies.

Two monoclonal antibodies (MoAb) to the Skalica virus from the tick-borne encephalitis (TBE) complex were used to compare Karshi and Royal Farm viruses with the Russian spring-summer encephalitis, Central European encephalitis (Hypr and Kumlinge strains) Skalica, Langat and Powassan viruses. The first MoAb was prepared by fusion of P3NS1 cells with BALB/c mouse spleen cells, immunized with the Skalica virus; it was of IgM class and reacted in haemagglutination-inhibition (HI) test (MoAb type 1). The second MoAb was of IgG class and reacted in complement-fixation (CF) test (MoAb type 2). MoAb type 1 reacted in the HI test with Russian spring-summer encephalitis (RSSE), Central European encephalitis (CEE) virus strains, Skalica and Langat viruses. No reaction was observed with Powassan, Karshi, and Royal Farm viruses. MoAb type 2 reacted in the CF test with all members of tick-borne encephalitis complex except the Powassan, Karshi, and Royal Farm viruses.

Animals↗
PubMed1987

[Acute viral meningitis and encephalitis in children].

Both viral meningitis and encephalitis in infants and children give clinical features of various severity. The mechanism of viral encephalitis varies from CNS cellular destruction, immune or oedematous process. The clinical and EEG features of herpes encephalitis in the child are usually well recognizable. CSF characteristics are important for differential diagnosis. Management therapy includes anti-oedema treatment, prevention or cure of seizures. Passive immunisation against rubella, rubeola and measles is the best prevention therapy for post-infectious encephalitis. Herpes encephalitis prognosis has improved with acyclovir therapy. In France, mortality due to post-infectious encephalitis is estimated below 5% and sequellae below 20%.

Acute Disease↗
PubMed1988

[Intracranial pressure in comatose meningitis and encephalitis in children].

To determine the importance of intracranial hypertension in central nervous system acute infections, we studied intracranial pressure (ICP) in 27 patients, aged 45 days to 13 years. Fourteen had meningitis and 13 had encephalitis; all were in deep coma with a Glasgow Coma Scale 7 or less. Intracranial hypertension defined by a mean ICP above 15 mm Hg was observed in 12 patients with meningitis (86%) and in 9 with encephalitis (69%). Patients with meningitis exhibited a very early and severe intracranial hypertension. A striking difference is noted between survivors and non-survivors who had a very high maximal ICP with a severe reduction in cerebral perfusion pressure. Intracranial hypertension occurred in all patients with acute primitive encephalitis but only in 3/7 patients with post-infectious encephalitis. ICP monitoring seems to be important in the comatose forms of bacterial meningitis in the early period, herpes encephalitis and postinfectious encephalitis with severe status epilepticus.

Adolescent↗
PubMed1995

Definitive identification of a gene that confers resistance against Toxoplasma cyst burden and encephalitis.

Control of resistance to cyst burden following per-oral infection with Toxoplasma gondii has been mapped previously to a region of mouse chromosome 17 of approximately 140 kb. This region is contiguous with and contains the class I gene, Ld. Resistance to development of toxoplasmic encephalitis has also been reported to be controlled by genes in this region of H-2. TNF-alpha, D and L genes, as well as unidentified genes, are also in this region. The work described here was performed to identify definitively the gene(s) in this 140 kb region that confers resistance to cysts and encephalitis. The study demonstrates that relative resistance to T. gondii organisms and cyst burden in brain, and toxoplasmic encephalitis, 30 days following per-oral T. gondii infection is correlated absolutely with the presence of the Ld gene in inbred, recombinant, mutant and C3H.Ld transgenic mice. Mice with the Ld gene had lower cyst burdens and less encephalitis than those without the Ld gene. Specifically, 30 days after infection mice with the Ld gene had minimal perivascular inflammation and meningeal inflammation and very few Toxoplasma cysts or organisms in immunoperoxidase-stained preparations of their brains. Mice without the Ld gene had a similar pattern of inflammation, but in addition they had collections of inflammatory cells in the brain parenchyma. Free tachyzoites were found within these foci of inflammation and cysts were present in these areas as well as in contiguous areas without inflammatory cells. There were CD4+ and CD8+ T lymphocytes in the areas of inflammation and throughout the brain parenchyma. Mice that were resistant to cysts and encephalitis had little detectable brain cytokine mRNA expression, while mice that were susceptible had elevated levels of mRNA for a wide range of cytokines, consistent with their greater amounts of inflammation. The present work definitively demonstrates that a Ld-restricted response decreases the number of organisms and cysts within the brain and thereby limits toxoplasmic encephalitis and levels of interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha), interleukin-2 (IL-2), IL-6, IL-10, transforming growth factor-beta (TGF-beta), IL-1 alpha, IL1 beta and macrophage inhibiting protein (MIP) mRNA in the brain 30 days after per-oral infection.

Animals↗