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

Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

20
Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins...
20
Pathophysiology of Vomiting01:22

Pathophysiology of Vomiting

4.5K
Vomiting is a complex physiological response to expel harmful or irritating substances from the body. It's a defensive mechanism triggered by stimuli like poisons, microbial toxins, cytotoxic drugs, and mechanical abdominal distension. The process is centrally coordinated by the vomiting (or emetic) center located in the medulla of the brainstem. This area, rich in muscarinic M1, histamine H1, neurokinin 1 (NK1), and serotonin 5-HT3 receptors, coordinates the act of vomiting through...
4.5K
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

24
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...
24
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

54
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...
54
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

22
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...
22
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

30
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...
30

You might also read

Related Articles

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

Sort by
Same author

Evidence that 5-HT<sub>2A</sub> receptor signalling efficacy and not biased agonism differentiates serotonergic psychedelic from non-psychedelic drugs.

British journal of pharmacologyยท2025
Same author

Dreaming of Better Treatments: Advances in Drug Development for Sleep Medicine and Chronotherapy.

Journal of sleep researchยท2025
Same author

Molecular components of the circadian clock regulate HIV-1 replication.

iScienceยท2023
Same author

Inhibition of salt inducible kinases reduces rhythmic HIV-1 replication and reactivation from latency.

The Journal of general virologyยท2023
Same author

Phase I Trial of Ipatasertib Plus Carboplatin, Carboplatin/Paclitaxel, or Capecitabine and Atezolizumab in Metastatic Triple-Negative Breast Cancer.

The oncologistยท2023
Same author

The multiple roles of salt-inducible kinases in regulating physiology.

Physiological reviewsยท2023

Related Experiment Video

Updated: May 2, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
10:39

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

Published on: June 2, 2014

19.1K

Migraine pathophysiology.

Mari Bozoghlanian1, Sridhar Vasudevan

  • 1Wisconsin Rehabilitation Medicine Professionals, SC PO Box 240860, Milwaukee, WI 53224, USA.

Pain Management
|March 21, 2014
PubMed
Summary

Migraine pain theories are evolving due to the lack of clear pathology. Current research explores peripheral and central nervous system origins for migraine genesis.

Area of Science:

  • Neurology
  • Neuroscience
  • Pain Research

Background:

  • Migraine pathophysiology remains incompletely understood, lacking identifiable cephalic pathology.
  • Current understanding is based on two primary theories regarding migraine pain origin.

Purpose of the Study:

  • To review the clinical presentation and diagnosis of migraine.
  • To explain traditional and current theories of migraine pathogenesis.

Main Methods:

  • Review of existing literature on migraine pathophysiology.
  • Analysis of peripheral and central nervous system theories.

Main Results:

  • Two main theories exist: peripheral activation of nociceptive neurons and central nervous system (CNS) origin due to abnormal sensory processing.

More Related Videos

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

4.7K
Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache
05:40

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Published on: July 29, 2021

8.6K

Related Experiment Videos

Last Updated: May 2, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
10:39

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

Published on: June 2, 2014

19.1K
Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
08:39

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents

Published on: May 16, 2022

4.7K
Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache
05:40

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Published on: July 29, 2021

8.6K
  • The absence of clear cephalic pathology complicates definitive understanding.
  • Conclusions:

    • Migraine pathogenesis theories continue to develop, encompassing both peripheral and central mechanisms.
    • Further research is needed to elucidate the exact mechanisms underlying migraine pain.