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Related Concept Videos

Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

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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...
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Encephalitis l: Introduction01:19

Encephalitis l: Introduction

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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...
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Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

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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...
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Hepatic Encephalopathy01:29

Hepatic Encephalopathy

46
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...
46
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

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A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial...
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Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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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...
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Septic encephalopathy: does inflammation drive the brain crazy?

Felipe Dal-Pizzol1, Cristiane D Tomasi1, Cristiane Ritter1

  • 1Laboratory of Experimental Pathophysiology and National Science and Technology Institute for Translational Medicine (INCT-TM), Graduate Program in Health Sciences, Health Sciences Research Center, Universidade do Extremo Sul Catarinense (UNESC), Criciúma, SC, Brazil.

Revista Brasileira De Psiquiatria (Sao Paulo, Brazil : 1999)
|June 12, 2014
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Summary
This summary is machine-generated.

Sepsis can cause brain dysfunction, known as sepsis-associated encephalopathy (SAE), by disrupting key brain chemicals called neurotransmitters. This review explores how inflammation during sepsis affects neurotransmitter metabolism, leading to SAE symptoms.

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Area of Science:

  • Neuroscience
  • Critical Care Medicine
  • Pathophysiology

Background:

  • Sepsis is a life-threatening condition causing organ dysfunction and high mortality.
  • Sepsis-associated encephalopathy (SAE) is an early neurological complication of sepsis.
  • Neurotransmitter deregulation, particularly acetylcholine, is hypothesized as a key pathway in SAE.

Purpose of the Study:

  • To review current evidence on how systemic inflammation impacts central nervous system (CNS) neurotransmitter metabolism.
  • To elucidate the mechanisms linking inflammation to SAE development.
  • To explain how systemic inflammation affects brain function during sepsis.

Main Methods:

  • Literature review of existing studies on sepsis, inflammation, and neurotransmitter function.
  • Analysis of evidence for inflammatory mechanisms affecting major CNS neurotransmitters.
  • Synthesis of findings to explain the pathophysiology of SAE.

Main Results:

  • Systemic inflammation during sepsis is strongly implicated in altering neurotransmitter metabolism.
  • Evidence suggests inflammation interferes with the synthesis, release, and reuptake of key neurotransmitters.
  • Specific neurotransmitter systems, including cholinergic pathways, are particularly vulnerable.

Conclusions:

  • Systemic inflammation plays a critical role in the development of sepsis-associated encephalopathy.
  • Understanding these inflammatory-neurotransmitter interactions is crucial for developing targeted therapies for SAE.
  • Further research is needed to fully elucidate the complex mechanisms involved.