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Related Concept Videos

Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...

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EEG Microstate Imbalance in Anti-LGI1 Encephalitis: A Correlation With Inflammation and Cognitive Dysfunction.

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    |September 25, 2025
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    Electroencephalogram (EEG) microstate alterations, including prolonged durations and altered transitions, are linked to inflammation and cognitive decline in anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis patients.

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    Area of Science:

    • Neuroscience
    • Neurology
    • Neuroimmunology

    Background:

    • Anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis is an autoimmune disorder affecting the brain.
    • Electroencephalogram (EEG) microstates offer insights into large-scale brain network dynamics.
    • The relationship between EEG microstate changes, inflammation, and cognitive deficits in anti-LGI1 encephalitis remains unclear.

    Purpose of the Study:

    • To investigate alterations in EEG microstates in patients with anti-LGI1 encephalitis.
    • To explore the correlation between these microstate changes, inflammatory markers, and cognitive function.

    Main Methods:

    • Resting-state EEG recordings from 30 anti-LGI1 encephalitis patients and 30 healthy controls.
    • Microstate analysis and functional connectivity assessment using EEGLAB and sLORETA.
    • Correlation analyses with inflammatory markers (NLR, SII, SIRI, dNLR) and cognitive scores (MMSE).

    Main Results:

    • Patients showed prolonged microstate A, B, C durations, reduced D occurrence, and altered C-to-A transitions.
    • Microstate A activity decreased in specific brain regions; functional connectivity showed altered slow-wave and fast-wave patterns.
    • Microstate alterations correlated significantly with inflammatory indices and inversely with cognitive function (MMSE scores).

    Conclusions:

    • EEG microstate analysis reveals significant alterations in patients with anti-LGI1 encephalitis.
    • The observed microstate imbalances, particularly the AD/BC ratio, are associated with systemic inflammation.
    • These EEG changes correlate with cognitive impairments, suggesting microstates as potential biomarkers for disease severity and progression.