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Related Concept Videos

Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
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...
Bacterial Meningitis01:24

Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.Routes of Entry...
Cerebral Edema ll: Pathophysiology01:22

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Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
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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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Related Experiment Video

Updated: Jul 1, 2026

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis
08:46

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis

Published on: August 12, 2020

Sepsis causes neuroinflammation and concomitant decrease of cerebral metabolism.

Alexander Semmler1, Sven Hermann, Florian Mormann

  • 1Department of Neurology, University Bonn, Bonn, Germany.

Journal of Neuroinflammation
|September 17, 2008
PubMed
Summary
This summary is machine-generated.

Septic encephalopathy (SE) impairs brain function through systemic inflammation, affecting cerebral blood flow and neuronal metabolism. This study reveals early neuronal dysfunction and inflammation in a rat model, offering insights for therapeutic strategies.

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Last Updated: Jul 1, 2026

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis
08:46

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Published on: August 12, 2020

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Area of Science:

  • Neuroscience
  • Immunology
  • Pathophysiology

Background:

  • Septic encephalopathy (SE) is severe brain dysfunction from systemic inflammation without direct brain infection.
  • It involves altered cerebral blood flow, inflammatory molecules, and metabolic changes, leading to neuronal dysfunction and death.

Purpose of the Study:

  • To investigate the relationship between electrophysiological, metabolic, and morphological changes in SE.
  • To understand the impact of bacterial lipopolysaccharide (LPS) on brain function.

Main Methods:

  • Simultaneous assessment of systemic circulation, regional cerebral blood flow, and cortical electroencephalography in rats exposed to LPS.
  • Small animal PET ([18F]FDG), immunohistochemistry, and real-time PCR were used to examine glucose uptake, glial activation, and inflammatory gene transcription.

Main Results:

  • Reduced cortical blood flow and alpha activity in EEG, alongside decreased cerebral glucose uptake in neocortical areas.
  • Increased transcription of pro- and anti-inflammatory cytokines and chemokines in the cerebrum.
  • Increased microglia activation and decreased neuronal cell counts in the cortex and hippocampus.

Conclusions:

  • Sepsis induces complex, early impairments in neuronal metabolism and activity.
  • The study's model, using clinically relevant techniques, may aid in developing brain-specific therapies for human SE.