Monitoring and tentative diagnosis of herpetic encephalitis by protein analysis of cerebrospinal fluid

Sindic, Christian; Kevers, Luc; Chalon, M.P.; Laterre, Emile-Christian; Masson, Pierre

doi:10.1016/0022-510x(85)90161-3

Cited by 11 publications

(5 citation statements)

References 25 publications

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“…A few studies on CNS infections have previously been conducted, studying meningitis (17 Á/19), encephalitis (18,20,21), fungal infections of the brain (19,22) and other aspects (23 Á/25). However, some of these studies are outdated and use older analysis kits, some deal only with CSF, some deal with other, less well documented, markers and 1 study involves animal models (22).…”

Section: Discussionmentioning

confidence: 99%

Serum S100B levels in patients with cerebral and extracerebral infectious disease

Undén

Christensson

Bellner

et al. 2004

Scandinavian Journal of Infectious Diseases

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S100B has been shown to increase in cerebrospinal fluid (CSF) and serum after various neurological diseases and it has been postulated that S100B could serve as a serum marker for brain damage. However there is limited information concerning serum S100B levels in infectious diseases of the brain. Blood samples were collected from patients at the Department of Infectious Diseases at or soon after admission. The different diagnoses studied were bacterial meningitis, pneumonia, viral meningitis, cerebral abscess, enteritis, erysipelas, viral encephalitis and neuroborreliosis. A serum S100B level > 0.15 microg/l was defined as increased. 57 patients were included in the study. S100B was elevated in 33% of patients (19/57). 73% (8/11) of patients with bacterial meningitis showed increased levels compared to 7% (1/14) of patients with viral meningitis. Viral encephalitis showed the highest mean S100B levels (mean 0.58 microg/l). 25% (6/24) of patients with extracerebral infections showed raised S100B levels. S100B levels were generally higher in patients with cerebral infections than in extracerebral infections. However, both false negative and false positive S100B levels were observed which may limit the use of S100B as a brain specific serum marker.

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Section: Discussionmentioning

confidence: 99%

Serum S100B levels in patients with cerebral and extracerebral infectious disease

Undén

Christensson

Bellner

et al. 2004

Scandinavian Journal of Infectious Diseases

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“…However, in this study, the correlation between the size of the ischemic area and the astroglial protein increment apparently was not investigated, and no correlation to the clinical outcome of these patients was found. 5 Even so, in studies concerning other cerebral disorders, such as herpes encephalitis 22 and subarachnoid hemorrhage, 23 -24 the S-100 concentration was found to be related to the clinical state, as well as to the outcome of the patient.…”

Section: Discussionmentioning

confidence: 99%

Determination of S-100 and glial fibrillary acidic protein concentrations in cerebrospinal fluid after brain infarction.

Aurell

Rosengren

Karlsson

et al. 1991

Stroke

200

123

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Background and Purpose:We initiated the present study to evaluate the clinical value of consecutive concentration determinations of S-100 and glial fibrillary acidic proteins in cerebrospinal fluid from patients with brain infarction.Methods: We took sequential samples of cerebrospinal fluid from 28 patients within 48 hours, at 7 days, and at 18-21 days after the ictus. We measured astroglial protein concentrations using an enzyme-linked immunosorbent assay and also determined size of the infarction (computed tomography), clinical state of the patient (simplified activities of daily living test), blood-brain barrier dysfunction (cerebrospinal fluid/serum albumin ratio), and a myelin marker (myelin basic protein). Results: We found a transient increase of both proteins in the cerebrospinal fluid during the first week after the ischemic stroke (/?<0.05). This increment was significantly correlated with the size of the infarction and the clinical state of the patients.Conclusions: Transient release of astroglial proteins into the cerebrospinal fluid possibly reflects initial focal ischemic damage and, in the later phase, ongoing destruction of astroglial cells in the penumbra zone. We suggest that determinations of cerebrospinal fluid astroglial protein concentrations can be used to estimate ischemic brain damage, which should be of particular value in clinical trials of pharmacological agents, such as calcium antagonists, on stroke patients. (Stroke 1991;22:1254-1258)

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“…Few patients with viral CNS infections have previously been studied with regard to neuronal and astroglial markers in CSF [20,23]. The extremely high maximum concentrations and the kinetics of the markers in HSV-1 encephalitis imply that they may be used as brain damage markers to follow individual patients longitudinally or to evaluate treatment strategies.…”

Section: Discussionmentioning

confidence: 99%

“…The high tissue concentration of S-100 makes it a useful CSF marker of astroglial cell damage. CSF GFAp and S-100 levels have been shown to increase after structural damage in the CNS as in stroke and encephalitis [19,20,23].…”

Section: Introductionmentioning

confidence: 99%

Difference in pathogenesis between herpes simplex virus type 1 encephalitis and tick-borne encephalitis demonstrated by means of cerebrospinal fluid markers of glial and neuronal destruction

Studahl¹,

Rosengren

Gunther

et al. 2000

Journal of Neurology

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We determined the extent of neuronal and glial cell destruction in 13 patients with herpes simplex type 1 (HSV-1) encephalitis, 15 patients with tick-borne encephalitis (TBE), and 20 noninfectious controls by analyzing the cerebrospinal fluid (CSF) concentrations of neurofilament protein (a marker of neurons, mainly axons), neuron-specific enolase (a marker of neurons, mainly somas), glial fibrillary acidic protein, and S-100 protein (markers of astrocytes). In addition, in patients with HSV-1 encephalitis CSF samples were collected serially before 7, 8-14, and 18-49 days and 3-10 months after the onset of neurological symptoms. In the acute stage of HSV-1 encephalitis we found markedly higher CSF levels of the cell damage markers than in patients with TBE. The concentration of cell damage markers in HSV-1 encephalitis decreased within 45 days after acute infection, except for neurofilament protein. The CSF concentrations of neurofilament protein increased during the second week, remained extremely high throughout the next month, and decrease thereafter. The changes in these markers of neuronal and glial destruction demonstrate the neuronal and astroglial cell damage during the first month after HSV-1 encephalitis. In contrast, most patients with TBE had signs only of slight astrogliosis, except for two patients with paresis.

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Monitoring and tentative diagnosis of herpetic encephalitis by protein analysis of cerebrospinal fluid

Cited by 11 publications

References 25 publications

Serum S100B levels in patients with cerebral and extracerebral infectious disease

Serum S100B levels in patients with cerebral and extracerebral infectious disease

Determination of S-100 and glial fibrillary acidic protein concentrations in cerebrospinal fluid after brain infarction.

Difference in pathogenesis between herpes simplex virus type 1 encephalitis and tick-borne encephalitis demonstrated by means of cerebrospinal fluid markers of glial and neuronal destruction

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