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PubMed1953

The 1952 outbreak of encephalitis in California; epidemiologic aspects.

For the most part, epidemiologic phenomena observed in the outbreak of encephalitis in 1952 accorded with patterns that had been apparent in previous years. Ninety-seven per cent of the 414 laboratory-confirmed cases of western equine and St. Louis encephalitis in humans occurred in the 20 Central Valley counties. The cases of western equine encephalomyelitis in horses were generally scattered over the state. In the Central Valley most of the cases in horses were in animals less than two years of age; elsewhere the incidence was higher in older horses.There were no laboratory-confirmed cases of western equine or St. Louis encephalitis in humans earlier than June or later than October. In 1952 there were far more cases of western equine than of St. Louis encephalitis-a departure from the pattern in the previous seven years when there were about as many of one as of the other. No known satisfactory index is available for the prediction of the extent or type of outbreaks in humans. Approximately one-third of the cases of western equine encephalitis were in patients less than one year of age, whereas there were no cases of the St. Louis disease in patients that young.The incidence of western equine encephalitis in persons under 5 years of age was about the same for girls as for boys. In higher age brackets, males with western equine encephalitis outnumbered females 2 to 1. The corresponding ratio for St. Louis encephalitis was only 1.2 to 1.

Animals↗
PubMed2000

Damage and repair of DNA in HIV encephalitis.

Neuronal damage and dementia are common sequelae of HIV encephalitis. The mechanism by which HIV infection of CNS macrophages results in neuronal damage is not known. We examined the brains from 15 AIDS autopsies (8 with HIV encephalitis and 7 without) and 4 non-infected control autopsies for the presence of DNA strand breaks, for associated changes in the expression of the DNA repair enzymes KU80 and Poly (ADP-ribose) polymerase (PARP), and for accumulation of amyloid precursor protein (APP). Abundant DNA damage was observed with terminal transferase-mediated dUTP nick end-labeling (TUNEL), however, there was no morphologic evidence of significant neuroglial apoptosis. The DNA repair enzyme KU80 was immunocytochemically detectable in neuronal and glial cells in autopsy brains from patients with and without HIV encephalitis; however, in cases with HIV encephalitis the staining was more prominent than in the infected or non-infected controls without encephalitis. There was no difference in KU80 immunostaining in oligodendroglia from autopsies with and without encephalitis. Immunostaining for PARP was more intense in gray and white matter of cases with HIV encephalitis. No clear spatial relationship existed between expression of DNA repair enzymes and the spatial proximity of microglial nodules or HIV-infected macrophages. The cytoplasm of cortical and subcortical neurons immunostained for APP Stronger cortical neuronal APP staining was observed in cases without HIV encephalitis. Staining of deep gray matter neurons was similar, irrespective of the presence or absence of encephalitis. While foci of intense APP staining were noted in white matter not related to HIV infection, they were associated with foci of opportunistic infections (e.g. due to CMV or PML). We conclude that damaged DNA and altered patterns of expression of DNA repair proteins and APP are common findings in the brains of AIDS patients at autopsy, but do not have a spatial relationship to HIV-infected macrophages.

AIDS Dementia Complex↗
PubMed2002

Relapsed and late-onset Nipah encephalitis.

An outbreak of infection with the Nipah virus, a novel paramyxovirus, occurred among pig farmers between September 1998 and June 1999 in Malaysia, involving 265 patients with 105 fatalities. This is a follow-up study 24 months after the outbreak. Twelve survivors (7.5%) of acute encephalitis had recurrent neurological disease (relapsed encephalitis). Of those who initially had acute nonencephalitic or asymptomatic infection, 10 patients (3.4%) had late-onset encephalitis. The mean interval between the first neurological episode and the time of initial infection was 8.4 months. Three patients had a second neurological episode. The onset of the relapsed or late-onset encephalitis was usually acute. Common clinical features were fever, headache, seizures, and focal neurological signs. Four of the 22 relapsed and late-onset encephalitis patients (18%) died. Magnetic resonance imaging typically showed patchy areas of confluent cortical lesions. Serial single-photon emission computed tomography showed the evolution of focal hyperperfusion to hypoperfusion in the corresponding areas. Necropsy of 2 patients showed changes of focal encephalitis with positive immunolocalization for Nipah virus antigens but no evidence of perivenous demyelination. We concluded that a unique relapsing and remitting encephalitis or late-onset encephalitis may result as a complication of persistent Nipah virus infection in the central nervous system.

Adolescent↗
PubMed1983

Relapsing herpes simplex encephalitis following antiviral therapy.

Although treatment for herpes simplex virus (HSV) encephalitis with antiviral agents has improved survival, occasional patients experience unexplained clinical exacerbations. This report presents evidence that some relapses may occur from recurrent viral encephalitis. An adult male developed the classic symptoms of HSV encephalitis. The cerebrospinal fluid (CSF), electroencephalogram, and isotope brain scan suggested a localized encephalitis involving the left temporal lobe. The patient was treated for 10 days with high doses of cytosine arabinoside instead of the currently recommended adenine arabinoside. Progression of encephalitis stopped, and clinical recovery occurred. The HSV antibody titer increased eightfold. Fifty-four days after the initial encephalitis, the patient relapsed with a subacute progressive encephalitis involving the same brain area. The CSF demonstrated oligoclonal bands, elevated immunoglobulin G levels (100 mg/dl), and a high HSV antibody titer (1:8,192 by indirect hemagglutination test). From a left temporal lobe biopsy taken 74 days after onset of the initial encephalitis, herpes simplex virus type 1 was isolated. Without renewed antiviral drug therapy, the patient slowly recovered.

Adult↗
PubMed2006

Beyond viruses: clinical profiles and etiologies associated with encephalitis.

BACKGROUND: Encephalitis is a complex syndrome, and its etiology is often not identified. The California Encephalitis Project was initiated in 1998 to identify the causes and further describe the clinical and epidemiologic characteristics of encephalitis. METHODS: A standardized report form was used to collect demographic and clinical data. Serum, cerebrospinal fluid, and respiratory specimens were obtained prospectively and were tested for the presence of herpesviruses, arboviruses, enteroviruses, measles, respiratory viruses, Chlamydia species, and Mycoplasma pneumoniae. The association between an identified infection and encephalitis was defined using predetermined, organism-specific criteria for confirmed, probable, or possible causes. RESULTS: From 1998 through 2005, a total of 1570 patients were enrolled. Given the large number of patients, subgroups of patients with similar clinical characteristics and laboratory findings were identified. Ten clinical profiles were described. A confirmed or probable etiologic agent was identified for 16% of cases of encephalitis: 69% of these agents were viral; 20%, bacterial; 7%, prion; 3%, parasitic; and 1%, fungal. An additional 13% of cases had a possible etiology identified. Many of the agents classified as possible causes are suspected but have not yet been definitively demonstrated to cause encephalitis; these agents include M. pneumoniae (n=96), influenza virus (n=22), adenovirus (n=14), Chlamydia species (n=10), and human metapneumovirus (n=4). A noninfectious etiology was identified for 8% of cases, and no etiology was found for 63% of cases. CONCLUSIONS: Although the etiology of encephalitis remains unknown in most cases, the recognition of discrete clinical profiles among patients with encephalitis should help focus our efforts toward understanding the etiology, pathogenesis, course, and management of this complex syndrome.

Adolescent↗
PubMed2005

Autoantibodies and cell-mediated autoimmunity to NMDA-type GluRepsilon2 in patients with Rasmussen's encephalitis and chronic progressive epilepsia partialis continua.

PURPOSE: To evaluate antibody-mediated and cytotoxic T cell-mediated pathogenicity that has been implicated as the autoimmune pathophysiological mechanism in Rasmussen's encephalitis. METHODS: We examined autoantibodies against the N-methyl-d-aspartate glutamate receptor (NMDA-type GluR) epsilon2 subunit and its epitopes in serum and CSF samples from 20 patients [five histologically proven (definitive) Rasmussen's encephalitis with epilepsia partialis continua (EPC), four definitive Rasmussen's encephalitis without EPC, and 11 clinical Rasmussen's encephalitis with EPC]. We examined 3H-thymidine uptake into lymphocytes after stimulation by GluRs. RESULTS: All nine definitive patients (five patients with EPC and four without EPC), and 10 of 11 clinical Rasmussen's encephalitis patients had the autoantibodies. In four patients, the autoantibodies were absent in early stage when epileptic seizures had already become frequent, and appeared subsequently. In two patients, the autoantibodies persisted in the serum after frontal lobe resection or functional hemispherectomy, although epileptic seizures were completely controlled. Autoantibodies to the C2 epitope predominated, while autoantibodies to the extracellular N epitope were rare. The mean 3H-thymidine uptake ratios (stimulation by GluRepsilon2-containing homogenates/stimulation by PHA) were significantly higher in definitive and clinical Rasmussen encephalitis patients than in controls. The mean 3H-thymidine uptake ratios (relative to PHA) were significantly higher for GluRepsilon2-containing homogenate than for control homogenate or GluRdelta2-containing homogenate. CONCLUSIONS: Autoantibodies against GluRepsilon2 may be one of the diagnostic markers for Rasmussen's encephalitis with and without EPC. Patients have activated T cells stimulated by GluRepsilon2 in peripheral blood circulation. We speculate that cellular autoimmunity and the subsequent humoral autoimmunity against GluRepsilon2 may contribute to the pathophysiological processes in Rasmussen's encephalitis.

Adolescent↗
PubMed1999

[Clinical study in 28 patients with infection-related acute onset encephalitis].

Of the 75 patients with infection-related acute encephalopathy or encephalitis treated by us in the last 10 years, 28 had acute onset encephalitis. The results of clinical studies on these 28 patients were as follows: (1) The number of cases who exhibited CNS manifestations during (A) and after pyrexia (B) were 15 and 13, and the ages of predilection were infancy and school age, respectively. (2) MRI studies in cases of A revealed multifocal CNS lesions in 1 case, localized lesions in 7 and normal findings in 7. In B, there were 3 cases with multifocal lesions, 8 of focal lesions and 2 of normal findings. (3) The 7 cases of localized lesions in A were divided into 5 of herpes encephalitis and 2 of suspected vasculitis. Vasculitis was suspected in 3 of 8 cases of localized lesions in B. Thus, vasculitis is considered to be an important cause of encephalitis. (4) Brain lesions in the 5 cases of herpes encephalitis were occipital dominant in 4. Only one case had a temporal lesion. (5) All cases with focal MRI lesions and CSF pleocytosis, having evidence of direct viral invasion, were herpes encephalitis. Direct viral invasion was not proven in any other cases. (6) Although the term encephalitis is often used in clinical practice, the process by which the CNS lesions occur in acute viral infection is still unknown. Therefore it is not easy to establish the diagnosis. The diagnostic criteria of encephalitis should be reconsidered. New specific methods to analyze the cause of CNS lesions are necessary.

Acute Disease↗
PubMed2005

[Japanese encephalitis].

Japanese encephalitis is an arboviral disease due to a flavivirus transmitted by a mosquito of the genus Culex. It is a major public health problem in Southeast Asia where it is endemo-epidemic. The socio-economic impact of Japanese encephalitis is great since most cases occur in children and young adults and lead to death in 25 to 30 % and neurological sequelae in survivors. The tendency of Japanese encephalitis to spread geographically and the existence of imported cases are particularly important issues. The clinical features are the same as other viral encephalitis. Suspicion of imported Japanese encephalitis depends on awareness of the epidemiological setting (return from endemic areas). Diagnosis must be confirmed by serology using ELISA capture method to detect anti-viral antibodies in blood and cerebrospinal fluid. Unlike herpes encephalitis, there is currently no specific treatment for Japanese encephalitis. Only preventive measures can be effective against infection. At the present time the most widely used vaccine is Biken's lyophilized vaccine produced from a reference strain (Nakayama strain), but its high cost prevents mass vaccination in endemic areas. Recent progress in molecular biology has raised hope for the discovery of a genetically engineered vaccine to improve overall protection against Japanese encephalitis.

Encephalitis, Japanese↗
PubMed1996

Atovaquone as long-term suppressive therapy for toxoplasmic encephalitis in patients with AIDS and multiple drug intolerance. Atovaquone Expanded Access Group.

OBJECTIVE: To evaluate the efficacy and tolerance of atovaquone used as long-term maintenance therapy in patients with toxoplasmic encephalitis and intolerant of conventional anti-Toxoplasma therapies. DESIGN: Uncontrolled open-label study of atovaquone given through an expanded access programme; statistical analysis was performed on an intent-to-treat basis. PATIENTS: Sixty-five patients intolerant of conventional toxoplasmic encephalitis therapies-pyrimethamine, sulphadiazine or clindamycin-received atovaquone as maintenance therapy after resolution of an acute episode of toxoplasmic encephalitis. Patients were clinically and neurologically evaluated monthly. Toxoplasmic encephalitis relapse was defined as the occurrence of neurological abnormalities, except in the case of a proven alternative diagnosis. RESULTS: Sixty-five patients were treated with atovaquone 750 mg four times daily and followed up for a mean period of 1 year. Mean CD4 lymphocytes count was 29 x 10(6)/l. Prior to starting atovaquone, patients had experienced a total of 129 episodes of intolerance to conventional anti-Toxoplasma drugs. Atovaquone was used as a single anti-toxoplasmic agent in 75% of the cases. Seventeen patients (26%) experienced a toxoplasmic encephalitis relapse. Sixty-three patients (97%) were able to tolerate and continued taking atovaquone. Two patients had to discontinue therapy because of side-effects. In a multivariate analysis, only the duration of pyrimethamine-sulphadiazine therapy during the acute therapy phase of toxoplasmic encephalitis was significantly associated with a decreased risk of toxoplasmic encephalitis relapse during maintenance therapy [relative risk, 0.64 for each week of pyrimethamine-sulphadiazine; 95% confidence interval (CI), 0.42-0.96; P = 0.03]. The survival probability was 70% at 1 year after the episode of toxoplasmic encephalitis (95% CI, 57-83). CONCLUSION: These results suggest that atovaquone is a well-tolerated alternative anti-Toxoplasma treatment for maintenance therapy in patients who are intolerant to conventional anti-Toxoplasma drugs.

Acquired Immunodeficiency Syndrome↗
PubMed2002

Primate encephalization and intelligence.

The amount of brain mass exceeding that related to an animal's total body mass is called encephalization. And quantifying encephalization has been argued to be directly related to an animal's level of intelligence. In this study, the legitimacy of the encephalization hypothesis was tested for encephalization slopes 0.28, 0.67, and 0.75 in Snell's equation of simple allometry by determining the intersexual encephalization similarity for humans and 18 other primate species and by comparing the encephalization quotients for humans and six other primate species against the learning ability evaluations for their intelligence. Results suggest that the most accurate means for quantifying the encephalization of humans and other adult primate species requires the use of Lapicque's universal exponent of 0.28 in Snell's equation of simple allometry. Since Lapicque's slope was derived from various vertebrate groups, this equation may potentially be universally applicable for determining relative adult vertebrate encephalization and intelligence.

Animals↗
PubMed1995

Australian X disease, Murray Valley encephalitis and the French connection.

Epidemics of a severe encephalitis occurred in eastern Australia between 1917 and 1925, in which over 280 cases were reported with a fatality rate of 68%. The disease had not been described previously and was called Australian X disease. The next epidemic occurred in south-east Australia in the summer of 1950-51. The disease was given its name of Murray Valley encephalitis as this was the area from which most cases were reported. A virus was isolated by Eric French in Victoria, and about the same time by John Miles and colleagues in South Australia. The virus Murray Valley encephalitis (MVE) virus, was shown to be a Group B arbovirus (flavivirus) which was related to, but distinct from, Japanese encephalitis virus. Early seroepidemiological studies showed that the most likely vertebrate hosts were water birds. MVE virus was first isolated from Culex annulirostris mosquitoes in 1960. The most recent epidemic of Murray Valley encephalitis occurred in 1974, at which time it was renamed Australian encephalitis. Since 1974, however, all cases have been confined to northern Australia, particularly the north of Western Australia. Indeed, the Kimberley region of Western Australia contains the only confirmed enzootic foci of virus activity. A closely related flavivirus, Kunjin virus, has also been shown to be an aetiological agent of Australian encephalitis. Since the first isolation of MVE and Kunjin viruses, considerable information has been accumulated on their ecology and epidemiology, some aspects of which are briefly described.

Animals↗
PubMed1996

[Acute encephalitis in children].

Acute encephalitis is mainly of viral origin. Two groups of are considered: i) primary encephalitis, such as Herpes simplex encephalitis with intra-thecal synthesis of antibodies, and ii) post-viral infection encephalitis or acute disseminated encephalitis with immune dysregulation. The most common clinical presentation (fever, consciousness disturbance and seizures) is not specific and may reveal bacterial meningitis or cerebral abscess which require a specific treatment. Acyclovir has allowed consistant advances in the treatment of herpes encephalitis. Vaccination against selected viral infection, such as measle vaccine, is the only way to prevent acute disseminated encephalitis.

Acute Disease↗
PubMed2001

Development of a simplified assay for the detection of neutralizing antibodies to Japanese encephalitis virus.

Japanese encephalitis virus is a common cause of viral encephalitis in Asia with an estimated 45,000 cases annually. It causes significant morbidity and mortality. It is transmitted primarily by Culex mosquitoes between birds and animals, while man is thought to be an accidental, dead-end host. Since dengue is also prevalent usually in Japanese encephalitis-endemic areas, all Japanese encephalitis positive sera must be confirmed by detecting Japanese encephalitis specific neutralizing antibodies. The plaque reduction neutralization test is the gold standard for detecting and quantifying Japanese encephalitis neutralizing antibodies. This test, however, takes about a week and is carried out in 6 or 24-well plates, which limits its usage for large-scale screening. A simplified assay was developed for the detection and quantification of Japanese encephalitis neutralizing antibodies. The assay, which is carried out in 96-well plates, would be suitable for use in the mass screening of the population's immunity level as well as for use in vaccine efficacy studies.

Animals↗
PubMed2002

Neuropathogenesis of Japanese encephalitis virus.

In the central nervous system, the Japanese encephalitis virus can replicate only in neurons. The mechanism of the type of neurotropism was analyzed. The susceptibility to Japanese encephalitis virus infection in the rat brain was closely associated with neuronal immaturity. The initial specific binding of the virus to cells is one of the reasons for neurotropism of the Japanese encephalitis virus. The treatment of Japanese encephalitis virus infection with the neutralizing monoclonal antibody against the E protein did not inhibit the virus from binding to the cell surfaces, but strongly inhibited Japanese encephalitis virus-induced cell fusion and internalization of the virus into the host cells. One of the genome regions responsible for neuropathogenesis of the Japanese encephalitis virus was located on the E protein-coding region. The 138th amino acid of the E protein was important for neuropathogenesis expression of the Japanese encephalitis virus. The cell fusion activity of the E protein was closely correlated with neuropathogenesis of the virus.

Animals↗
PubMed2026

Rashless varicella-zoster virus encephalitis diagnosed by metagenomic next-generation sequencing: two case reports.

BACKGROUND: Varicella-zoster virus (VZV) can cause a range of central nervous system (CNS) infections, but early diagnosis is difficult when typical skin rash is absent. Rashless VZV encephalitis may present with nonspecific clinical, cerebrospinal fluid (CSF), and neuroimaging findings and can mimic autoimmune encephalitis, primary central nervous system lymphoma, or other disorders. We report two cases of rashless VZV encephalitis diagnosed by CSF metagenomic next-generation sequencing (mNGS), with subsequent neurological complications. CASE PRESENTATION: Case 1 was a 68-year-old man admitted with fever, seizures, and impaired consciousness. Brain magnetic resonance imaging (MRI) showed multifocal abnormal signals. CSF analysis revealed marked pleocytosis and elevated protein levels, and CSF cytology showed suspected atypical lymphocytes, leading to early consideration of autoimmune encephalitis and primary central nervous system lymphoma. CSF mNGS detected VZV, and rashless VZV encephalitis was diagnosed. The patient improved after intravenous acyclovir combined with a short course of dexamethasone. On day 45 after disease onset, follow-up MRI showed a new acute cerebral infarction adjacent to the posterior horn of the left lateral ventricle. Recurrent CSF pleocytosis and persistent protein elevation suggested possible VZV-associated vasculopathy. After repeated antiviral treatment, he improved again, and no recurrence was observed during more than 3 years of follow-up. Case 2 was a 74-year-old man admitted with fever, low back pain, vomiting, and impaired consciousness. Brain MRI showed multifocal abnormal signals, and CSF analysis revealed marked inflammatory changes. CSF mNGS detected VZV, supporting the etiological diagnosis of rashless VZV encephalitis. The patient improved after intravenous acyclovir combined with a short course of dexamethasone. On day 14 after disease onset, he developed urinary retention, impaired defecation sensation, and bilateral lower-limb weakness, suggesting possible lumbosacral nerve root or cauda equina involvement. Suspected VZV-related Elsberg syndrome was considered. His urinary and bowel dysfunction recovered at 2 months after disease onset. CONCLUSIONS: Rashless VZV encephalitis may be diagnostically challenging because early clinical, CSF, and neuroimaging findings are nonspecific. CSF mNGS can support etiological diagnosis, and careful follow-up is needed to detect delayed vascular and lumbosacral nerve root complications.

Humans↗
PubMed2006

A single siRNA suppresses fatal encephalitis induced by two different flaviviruses.

BACKGROUND: Japanese encephalitis virus (JEV) and West Nile virus (WNV) are neurotropic flaviviruses that can cause acute encephalitis with a high fatality rate. Currently there is no effective treatment for these infections. METHODS AND FINDINGS: We tested RNA interference (RNAi)-based intervention to suppress lethal JE and WN encephalitis in mice. To induce RNAi, we used either lentivirally expressed short hairpin RNA (shRNA) or synthetic short interfering RNA (siRNA). As target, we selected the cd loop-coding sequence in domain II of the viral Envelope protein, which is highly conserved among all flaviviruses because of its essential role in membrane fusion. Using as a target a species-specific sequence in the cd loop that is conserved only among the different strains of either JEV or WNV, we could achieve specific protection against the corresponding virus. However, by targeting a cross-species conserved sequence within the cd loop, we were able to protect mice against encephalitis induced by both viruses. A single intracranial administration of lentivirally delivered shRNA or lipid-complexed siRNA before viral challenge or siRNA treatment after viral challenge was sufficient for protection against lethal encephalitis. CONCLUSIONS: RNAi-based intervention affords near complete protection from both JEV- and WNV- induced encephalitis in mice. Our results show, to our knowledge for the first time, that siRNA can be used as a broad-spectrum antiviral agent for treating encephalitis caused by multiple related viruses.

Animals↗
PubMed2006

A study of CSF catecholamine and its metabolites in acute and convalescent period of encephalitis.

AIMS: To evaluate cerebrospinal fluid (CSF) catecholamine (CA) and its metabolites in encephalitis patients in acute and convalescent period and correlate these with clinical and magnetic resonance imaging (MRI) features. SUBJECTS AND METHODS: Patients with acute encephalitis diagnosed on the basis of clinical, CSF, MRI and virological parameters underwent detailed neurological evaluation including Glasgow Coma Scale (GCS), Unified Parkinson's Disease Rating Scale (UPDRS) and Dystonia Rating Scale. Cranial MRI was carried out and CSF dopamine (DA), norepinephrine (NE), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxytryptamine (5HT) levels were estimated by High Performance Liquid Chromatography (HPLC). The CSF catecholamine levels were compared with convalescent phase as well as with controls. These levels were also correlated with parkinsonian features, dystonia and radiological abnormalities. RESULTS: There were 29 encephalitis patients; whose age ranged between 2 and 65 years, 4 were females and 11 children. 25 patients had Japanese encephalitis (JE) and 4 nonspecific encephalitis. The mean GCS score was 8 and 13 had seizures. Movement disorders were present in 13 patients and included parkinsonian features in 5, dystonia in 1 and combination of both in 7 patients. MRI revealed abnormalities in 15 out of 21 patients and included thalamic lesion in 10, globus pallidus in 4, putamen in 5, caudate in 4 and midbrain in 9 patients. In acute stage NE, DOPAC, 5HT and HVA levels were significantly lower compared to controls. NE levels significantly correlated with dystonia and thalamic lesions. Convalescent CSF study revealed significantly lower levels of DOPAC compared to acute phase. CSF catecholamine levels in encephalitis patients with and without movement disorders were not significantly different. CONCLUSION: In encephalitis, catecholamine and its metabolites are lower in acute and convalescent phase. Norepinephrine level correlates with dystonia and thalamic lesions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

[Viral encephalitis. Experiences with 53 patients in Middle Hessia].

Clinical symptoms, course of disease, cerebrospinal fluid (CSF) and cranial CT of 53 patients suffering from acute or subacute encephalitis were evaluated retrospectively. The virus could be identified in 21 (39%) patients. Nine of them had herpes simplex virus-encephalitis. 16 patients, eight with herpes simplex virus-encephalitis, died due to the disease. Complete restitution could be observed in 73% of survivors. Disturbance of consciousness and severe focal neurological deficit worsened prognosis towards letality and functional recovery. Most patients had initially elevated number of cellular elements and/or pathological protein concentration in CSF. CSF protein profile showed disturbance of blood-CSF-barrier function in a great number of patients during the first week of the disease whereas autochthonous production of immunoglobulin G was observed predominantly during the second and third week. Elevated concentration of CSF-lactate was seen in herpes simplex virus-encephalitis and in letal cases. 28 (53%) patients had pathological CT-findings. Generalized brain edema, focal hypodensities, focal and cortical contrast enhancement and hemorrhagic imbibation were observed. With one exception patients with herpes simplex virus-encephalitis had hypodense lesions in the temporal lobe. Besides this CT-findings did not allow conclusions regarding the etiology of encephalitis. Prognosis of encephalitis caused by other than herpes simplex virus was worse in case of pathological CT.

Acquired Immunodeficiency Syndrome↗