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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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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Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
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Published on: May 27, 2022

Pathophysiology-driven neuroimaging: decoding brain injury in sepsis.

Rui Yan1, Guanghui Ma2, Haixia Huang2

  • 1Department of Critical Care Medicine, Huashan Hospital, Fudan University, Shanghai, China.

Frontiers in Molecular Neuroscience
|June 30, 2026
PubMed
Summary
This summary is machine-generated.

Sepsis-associated encephalopathy (SAE) is brain dysfunction from sepsis, causing cognitive issues. Neuroimaging advances aid in diagnosing, predicting, and targeting treatments for this condition.

Keywords:
blood–brain barrierneuroimagingneuroinflammationsepsissepsis-associated encephalopathy

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Area of Science:

  • Neurology
  • Radiology
  • Critical Care Medicine

Background:

  • Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis, leading to diffuse brain dysfunction.
  • SAE is associated with high mortality rates and significant long-term cognitive deficits.
  • Pathogenesis involves endothelial activation, blood-brain barrier disruption, neuroinflammation, and neurotransmitter imbalance.

Purpose of the Study:

  • To review recent advancements in neuroimaging for SAE.
  • To integrate clinical, pathophysiological, and experimental findings.
  • To highlight the diagnostic, prognostic, and therapeutic potential of neuroimaging in SAE.

Main Methods:

  • Review of recent literature on neuroimaging in SAE.
  • Integration of clinical findings with pathophysiological and experimental evidence.
  • Analysis of emerging imaging modalities and their applications.

Main Results:

  • Neuroimaging provides critical insights into SAE's pathological features.
  • Imaging phenotypes correlate with underlying pathophysiological mechanisms.
  • Advances offer tools for early diagnosis and prognostic stratification.

Conclusions:

  • Neuroimaging plays a crucial role in understanding and managing SAE.
  • Emerging imaging techniques show translational potential for SAE.
  • Further research integrating imaging with clinical data is warranted.