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

Viral Meningitis01:18

Viral Meningitis

219
Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
219
Arboviral Encephalitis01:25

Arboviral Encephalitis

70
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...
70
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

32
Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
32
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

49
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...
49
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

29
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...
29
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

32
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...
32

You might also read

Related Articles

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

Sort by
Same author

A Qualitative Exploration of Paid Carers' Experience of Caring for Men With Intellectual and/or Developmental Disability and Harmful Sexual Behaviour.

Journal of applied research in intellectual disabilities : JARID·2026
Same author

Adenotonsillectomy is associated with increased risk and disease activity in pediatric-onset multiple sclerosis.

Multiple sclerosis (Houndmills, Basingstoke, England)·2026
Same author

The Development and Validation of Models of Risk for Behaviours That Challenge in Children With Developmental Disabilities: A Novel Machine Learning Approach.

Journal of intellectual disability research : JIDR·2026
Same author

The crystal structure of human transport and Golgi organization 2 homolog (TANGO2) suggests a cysteine N-terminal nucleophile (Ntn) hydrolase.

Acta crystallographica. Section D, Structural biology·2026
Same author

Severe Hyponatremia Presenting With Mild Symptoms and Multifactorial Etiology.

Journal of community hospital internal medicine perspectives·2026
Same author

Biomechanical Analysis of Lower Limb in Bharatanatyam Dance Using Musculoskeletal Modeling.

Indian journal of occupational and environmental medicine·2026

Related Experiment Video

Updated: May 6, 2026

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis
08:20

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis

Published on: June 2, 2022

3.1K

NMOSD: Previously Seropositive Patient Presents with Seronegative Brainstem Attack (P11-14.017).

Andrew Weber1, John Rose2, L DeWitt3

  • 1University of Utah.

Neurology
|February 20, 2025
PubMed
Summary

A patient with prior aquaporin-4 IgG (AQP4-IgG) positive neuromyelitis optica spectrum disorder experienced a relapse despite being seronegative for AQP4-IgG. This case highlights the potential for seronegative relapses in NMOSD and raises questions about antibody fluctuation and cellular immunity.

More Related Videos

Author Spotlight: Studying Neuroinflammatory Pathways Through Simultaneous Isolation of All Main CNS-Resident Cell Types
08:49

Author Spotlight: Studying Neuroinflammatory Pathways Through Simultaneous Isolation of All Main CNS-Resident Cell Types

Published on: October 6, 2023

1.6K
Author Spotlight: Advancing Immune Monitoring in Critical Care Patients Using Whole Blood Assays
06:03

Author Spotlight: Advancing Immune Monitoring in Critical Care Patients Using Whole Blood Assays

Published on: September 20, 2024

1.1K

Related Experiment Videos

Last Updated: May 6, 2026

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis
08:20

Hippocampal Neuronal Cultures to Detect and Study New Pathogenic Antibodies Involved in Autoimmune Encephalitis

Published on: June 2, 2022

3.1K
Author Spotlight: Studying Neuroinflammatory Pathways Through Simultaneous Isolation of All Main CNS-Resident Cell Types
08:49

Author Spotlight: Studying Neuroinflammatory Pathways Through Simultaneous Isolation of All Main CNS-Resident Cell Types

Published on: October 6, 2023

1.6K
Author Spotlight: Advancing Immune Monitoring in Critical Care Patients Using Whole Blood Assays
06:03

Author Spotlight: Advancing Immune Monitoring in Critical Care Patients Using Whole Blood Assays

Published on: September 20, 2024

1.1K

Area of Science:

  • Neurology
  • Immunology
  • Neuroimmunology

Background:

  • Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune condition characterized by antibodies against aquaporin-4 (AQP4-IgG).
  • NMOSD attacks can manifest as optic neuritis, transverse myelitis, or area postrema syndrome, and symptoms may occur independently or concurrently.

Purpose of the Study:

  • To describe a case of a patient with a history of AQP4-IgG seropositive NMOSD who experienced a new brainstem attack while seronegative for AQP4-IgG.
  • To explore the implications of seronegative relapses in NMOSD.

Main Methods:

  • Retrospective chart review, laboratory testing (ELISA, CBA-IFA, CBA-FACS), and brain MRI were utilized.
  • Longitudinal analysis of AQP4-IgG titers over time and during relapse was performed.

Main Results:

  • A 43-year-old female with NMOSD, initially AQP4-IgG positive, experienced a brainstem attack (area postrema syndrome) seven years after treatment cessation and when AQP4-IgG testing was negative.
  • MRI revealed a new enhancing posterior brainstem lesion, and symptoms resolved with IV methylprednisolone and plasma exchange.
  • A retrospective analysis indicated that 11% of seropositive patients in a study cohort became seronegative, often with low initial titers.

Conclusions:

  • This case demonstrates a seronegative relapse in NMOSD, challenging the traditional understanding of serostatus in disease activity.
  • The findings prompt further investigation into natural antibody fluctuations, antigenic spread, and the role of cellular immunity in seronegative NMOSD attacks.
  • The patient fulfilled criteria for seropositive NMOSD in 2012 and seronegative NMOSD in 2021.