Diagnostic approach and update on encephalitis

Bhimraj, Adarsh; Hasbun, Rodrigo

doi:10.1097/qco.0000000000000832

Cited by 5 publications

(2 citation statements)

References 19 publications

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“…An extensive serum- and CSF-diagnostic panel for differential diagnosis of encephalitis was repeated with additional diagnostic lumbar punctures on days 6, 20, and 33 ( 8 , 12 , 13 ). CSF showed a progressive lymphocytosis (increase of CSF cells at 13, 40, and 110, respectively, with >70% lymphocytes), progressive increase of total protein levels (49.7, 113, and 142 mg/dL for days 6, 20, and 33 respectively), lactate increase (3.1, 5.3, and 6.1 mmol/L respectively), increased IgG intrathecal production (53, 99, and 315 mg/dL), and constantly normal glucose.…”

Section: Case Descriptionmentioning

confidence: 99%

Case report: Fatal Borna virus encephalitis manifesting with basal brain and brainstem symptoms

Lourbopoulos,

Schnurbus,

Guenther

et al. 2024

Front. Neurol.

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BackgroundSince the first report of fatal Borna virus-1 (BoDV-1) encephalitis in 2018, cases gradually increased. There is a lack of diagnostic algorithm, and there is no effective treatment so far.Case presentationWe report an acute BoDV-1 encephalitis in a 77-year-old female with flu-like onset, rapid progression to word-finding difficulties, personality changes, global disorientation, diffuse cognitive slowness, and gait ataxia and further deterioration with fever, meningism, severe hyponatremia, epileptic seizures, cognitive decline, and focal cortical and cerebellar symptoms/signs. The extensive diagnostic workup (cerebrovascular fluid, serum, and MRI) for (meningo-)encephalitis was negative for known causes. Our empirical common antiviral, antimicrobial, and immunosuppressive treatment efforts failed. The patient fell into coma 5 days after admission, lost all brainstem reflexes on day 18, remained fully dependent on invasive mechanical ventilation thereafter and died on day 42. Brain and spinal cord autopsy confirmed an extensive, diffuse, and severe non-purulent, lymphocytic sclerosing panencephalomyelitis due to BoDV-1, affecting neocortical, subcortical, cerebellar, neurohypophysis, and spinal cord areas. Along with our case, we critically reviewed all reported BoDV-1 encephalitis cases.ConclusionThe diagnosis of acute BoDV-1 encephalitis is challenging and delayed, while it progresses to fatal. In this study, we list all tried and failed treatments so far for future reference and propose a diagnostic algorithm for prompt suspicion and diagnosis.

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Section: Case Descriptionmentioning

confidence: 99%

Case report: Fatal Borna virus encephalitis manifesting with basal brain and brainstem symptoms

Lourbopoulos,

Schnurbus,

Guenther

et al. 2024

Front. Neurol.

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“…An extensive diagnostic panel was repeated [6][7][8]. Any potential viral or bacterial causes were excluded by laboratory testing (PCR or IgM/IgG serology in serum and/or CSF).…”

Section: Introductionmentioning

confidence: 99%

A potential role for early hyponatremia in the diagnosis of Borna-virus encephalitis?

Lourbopoulos

Schnurbus

Guenther

et al. 2023

Preprint

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Background The first case of fatal Borna Virus-1 encephalitis (BoDV-1) was reported in 2018. Here, we report another fatal case of BoDV-1 encephalitis with early severe hyponatremia, indicative of neurohypophysial dysfunction. Case presentation: A 77-year-old female living in southern Germany was admitted to hospital in 2020 due to rapidly progressing word-finding difficulties, personality changes, global disorientation, diffuse cognitive slowness, and gait ataxia, initially without fever. After a rapid deterioration with fever, gait instability and ataxia, rapid cognitive decline, meningism, epileptic seizures, aphasia, and signs of latent right hemiparesis, the suspicion of a (meningo-)encephalitis was set. Furthermore, an unexplained, severe hyponatremia had been present since admission. Laboratory workup in cerebrovascular fluid (CSF) and serum as well as brain imaging was negative. Despite extensive empirical antiviral, antimicrobial, and immunosuppressive treatment efforts, the patient fell into coma (day 5), lost all brainstem functions (day 18), and remained fully dependent on invasive mechanical ventilation. Finally, she clinically developed a status of brain death and died 42 days after initial admission. Brain autopsy confirmed an extensive, diffuse, and severe affection of neocortical, subcortical and cerebellar structures as well as the neurohypophysis due to infection with BoDV-1. In light of the autopsy results, the hyponatremia could imply an early basal brain involvement, which could narrow down the initial differential diagnosis. Conclusion The diagnosis of BoDV-1 encephalitis remains clinically challenging. The disease progresses quickly to irreversible brain damage. An early, unexplained, hyponatremia in the presence of severe and rapidly evolving encephalitis may narrow down the diagnosis.

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Soluble Membrane Attack Complex (sMAC) as a Potential Diagnostic Biomarker Differentiating Acute Viral Encephalitis from Guillain-Barré Syndrome, a Post-infectious Autoimmune State

Swaminathan,

Varamballi,

Marate

et al. 2024

Curr Microbiol

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Diagnostic approach and update on encephalitis

Cited by 5 publications

References 19 publications

Case report: Fatal Borna virus encephalitis manifesting with basal brain and brainstem symptoms

Case report: Fatal Borna virus encephalitis manifesting with basal brain and brainstem symptoms

A potential role for early hyponatremia in the diagnosis of Borna-virus encephalitis?

Soluble Membrane Attack Complex (sMAC) as a Potential Diagnostic Biomarker Differentiating Acute Viral Encephalitis from Guillain-Barré Syndrome, a Post-infectious Autoimmune State

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