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

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...
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...
Arboviral Encephalitis01:25

Arboviral Encephalitis

Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
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...
Cryptococcal Meningitis01:27

Cryptococcal Meningitis

Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...
Leishmaniasis01:30

Leishmaniasis

Leishmaniasis is a protozoal disease caused by species of the genus Leishmania and transmitted through the bite of infected female sandflies. The parasite exists in two principal morphological forms during its life cycle. A sandfly acquires intracellular amastigotes from an infected reservoir host, such as a dog. Within the sandfly, these forms differentiate into motile, flagellated promastigotes. During a subsequent blood meal, promastigotes are injected into the human host, where they...

You might also read

Related Articles

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

Sort by
Same author

A JAK of All Trades: The Use of JAKi in a Patient With Erythema Annulare Centrifugum.

Cureus·2025
Same author

How We Do It: Sizing Split-Thickness Skin Grafts: The Stamp Method.

Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.]·2024
Same author

Double vision due to lateral rectus injury after cosmetic botulinum toxin injections.

The Australasian journal of dermatology·2023
Same author

Dupilumab as treatment for atopic dermatitis in a pediatric heart transplant patient: A case report.

Dermatologic therapy·2020
Same author

Examination of Treatment Satisfaction Instruments in Psoriasis: 2017 Results from the Psoriasis Working Group of the International Dermatology Outcome Measures (IDEOM).

Dermatology (Basel, Switzerland)·2020
Same author

The musician's mark.

JAAD case reports·2018
Same journal

Adverse Childhood Experiences and Pediatric Dermatology: Implications for Care, Equity, and Research.

Pediatric dermatology·2026
Same journal

State-of-the-Art Review: Vaccination in Pediatric Dermatology Patients Receiving Immunosuppressive or Immunomodulatory Therapy: A Review.

Pediatric dermatology·2026
Same journal

Multisystem Mucosal Morbidity in Recessive Dystrophic Epidermolysis Bullosa Inversa.

Pediatric dermatology·2026
Same journal

Infantile Transient Smooth Muscle Contraction of the Skin in Two Sisters.

Pediatric dermatology·2026
Same journal

Are 2021 CMS Changes Enough to Address the Pediatric Dermatology Crisis?

Pediatric dermatology·2026
Same journal

Annular Eruption in 12-Year-Old Boy.

Pediatric dermatology·2026
See all related articles

Related Experiment Video

Updated: Jun 6, 2026

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

Segmental vitiligo following encephalitis.

Angela Singh1, Heather Kornmehl, Sandy Milgraum

  • 1Internal Medicine Department, Robert Wood Johnson Medical School, New Brunswick, NJ, USA. angelasingh16@gmail.com

Pediatric Dermatology
|November 17, 2010
PubMed
Summary
This summary is machine-generated.

A rare case links viral encephalitis to segmental vitiligo, suggesting a neuronal role in vitiligo development. This finding supports the neuronal hypothesis for this skin depigmentation condition.

More Related Videos

Simultaneous Isolation of Principal Central Nervous System-Resident Cell Types from Adult Autoimmune Encephalomyelitis Mice
08:49

Simultaneous Isolation of Principal Central Nervous System-Resident Cell Types from Adult Autoimmune Encephalomyelitis Mice

Published on: October 6, 2023

Related Experiment Videos

Last Updated: Jun 6, 2026

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

Simultaneous Isolation of Principal Central Nervous System-Resident Cell Types from Adult Autoimmune Encephalomyelitis Mice
08:49

Simultaneous Isolation of Principal Central Nervous System-Resident Cell Types from Adult Autoimmune Encephalomyelitis Mice

Published on: October 6, 2023

Area of Science:

  • Neurology
  • Dermatology
  • Immunology

Background:

  • Vitiligo is a chronic autoimmune condition characterized by skin depigmentation.
  • The pathogenesis of vitiligo is complex and multifactorial, involving genetic and environmental factors.
  • Segmental vitiligo, a subtype, often presents with a unilateral, dermatomal distribution.

Observation:

  • A rare case of segmental vitiligo developing months after viral encephalitis is presented.
  • The patient's vitiligo followed a distinct dermatomal pattern.
  • No other precipitating factors for vitiligo were identified.

Findings:

  • The temporal association suggests a potential link between viral encephalitis and the onset of segmental vitiligo.
  • This case supports the neuronal hypothesis, proposing that nerve pathways may influence melanocyte function in vitiligo.
  • The findings warrant further investigation into neuro-immune interactions in vitiligo pathogenesis.

Implications:

  • Understanding the neuronal role in vitiligo could lead to novel therapeutic strategies.
  • This case highlights the importance of considering neurological events in the differential diagnosis of vitiligo.
  • Further research into the neuro-immune axis in vitiligo is crucial for advancing treatment options.