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Related Concept Videos

Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

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 with...
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...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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 barrier loses...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

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...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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...
Pathophysiology of Vomiting01:22

Pathophysiology of Vomiting

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 interaction...

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Related Experiment Video

Updated: Jul 4, 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

Migraine with and without aura share the same pathogenic mechanisms.

R Allan Purdy1

  • 1Department of Medicine, Dalhousie University, Halifax, Canada. a.purdy@dal.ca

Neurological Sciences : Official Journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
|July 17, 2008
PubMed
Summary

Migraine with and without aura likely share the same underlying causes. Research suggests a common pathophysiology for all migraine types, implying silent aura may occur in migraine without aura patients.

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Investigating Migraine-Like Behavior Using Light Aversion in Mice
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Investigating Migraine-Like Behavior Using Light Aversion in Mice

Published on: August 11, 2021

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Last Updated: Jul 4, 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

Investigating Migraine-Like Behavior Using Light Aversion in Mice
05:23

Investigating Migraine-Like Behavior Using Light Aversion in Mice

Published on: August 11, 2021

Area of Science:

  • Neurology
  • Neuroscience
  • Pathophysiology

Background:

  • Migraine with aura and without aura are distinct clinical classifications.
  • The headache characteristics are similar between migraine subtypes.
  • The presence or absence of aura is the primary differentiator.

Purpose of the Study:

  • To explore the shared pathogenic mechanisms between migraine with aura and migraine without aura.
  • To investigate the potential for clinically silent aura in patients with migraine without aura.
  • To propose a unified understanding of migraine pathophysiology.

Main Methods:

  • Review of neuroimaging studies on aura generation.
  • Clinical analysis of migraine subtypes.
  • Pathophysiological modeling of migraine events.

Main Results:

  • Emerging evidence from imaging studies clarifies aura generation mechanisms.
  • A common migraine pathophysiology for all subtypes appears plausible.
  • Migraine subtypes represent perturbations of normal physiology using standard anatomic pathways.

Conclusions:

  • Migraine with aura and migraine without aura likely share common pathogenic mechanisms.
  • The concept of clinically silent aura in migraine without aura warrants consideration.
  • A uniform pathogenesis underlies all clinical presentations of migraine.