Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

19
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...
19
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

11
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...
11
Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

1.1K
Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
1.1K
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

2
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...
2
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

4
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous...
4
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

5
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...
5

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

From dysbiosis to metabolic vulnerability: implications for precision psychiatry in depression.

Molecular psychiatry·2026
Same author

Toward a systems model of catatonia: Circuits, neurochemistry, immune perturbation, and biological heterogeneity.

Progress in neuro-psychopharmacology & biological psychiatry·2026
Same author

Hospital-treated infection associated with Alzheimer's disease pathology: underlying mechanisms.

Molecular psychiatry·2026
Same author

Impact of prenatal LPS on sepsis-related neurobiological outcomes.

Metabolic brain disease·2026
Same author

Emerging Therapeutic Interventions for Treatment‑Resistant Depression.

Advances in experimental medicine and biology·2026
Same author

Maternal exposure to sucrose and maltodextrin alters metabolism and genotoxicity in mice offspring.

Mutation research·2026

Related Experiment Video

Updated: Apr 22, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

20.4K

Mechanisms underlying uremic encephalopathy.

Giselli Scaini1, Gabriela Kozuchovski Ferreira1, Emilio Luiz Streck1

  • 1Laboratório de Fisiopatologia Experimental, Programa de Pós-graduação em Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brasil.

Revista Brasileira De Terapia Intensiva
|October 11, 2014
PubMed
Summary

Uremic encephalopathy in renal failure is complex, involving hormonal issues, oxidative stress, and neurotransmitter imbalances. Antioxidant therapy shows promise as an adjuvant treatment for these neurological complications.

More Related Videos

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
04:23

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

Published on: April 28, 2019

6.4K
Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

7.4K

Related Experiment Videos

Last Updated: Apr 22, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

20.4K
A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
04:23

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease

Published on: April 28, 2019

6.4K
Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

7.4K

Area of Science:

  • Nephrology
  • Neurology
  • Biochemistry

Background:

  • Encephalopathy is a common neurological complication in patients with renal failure.
  • Causes include uremia, thiamine deficiency, dialysis complications, and drug toxicity.
  • Symptoms progress from mild confusion to delirium and coma.

Purpose of the Study:

  • To review the mechanisms underlying the pathophysiology of uremic encephalopathy.
  • To discuss contributing factors and potential therapeutic strategies.

Main Methods:

  • Literature review of studies on uremic encephalopathy.
  • Analysis of postulated pathophysiological mechanisms.

Main Results:

  • The pathophysiology of uremic encephalopathy is multifactorial and not fully understood.
  • Key factors include hormonal disturbances, oxidative stress, metabolite accumulation, neurotransmitter imbalance, and metabolic disturbances.
  • Neurological complications often do not fully resolve with dialysis and can be exacerbated by treatment.

Conclusions:

  • Uremic encephalopathy involves complex pathophysiological pathways.
  • Antioxidant therapy may serve as an effective adjuvant treatment for neurological complications associated with renal failure.