Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Ischemic Stroke ll: Pathophysiology

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...

Hemorrhagic Stroke ll: Pathophysiology

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...

Stroke: Introduction and Types

Stroke: Introduction and Types

A stroke is an acute neurological event caused by the sudden disruption of cerebral blood flow, leading to rapid loss of neuronal function. Neurons depend on continuous oxygen and glucose supply, so even brief interruptions can cause irreversible injury within minutes. Strokes are classified into ischemic and hemorrhagic types.Ischemic StrokeIschemic strokes are most common and occur due to arterial occlusion, depriving brain tissue of oxygen and nutrients. This leads to energy failure, ionic...

Transient Ischemic Attack l: Introduction

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...

Ischemic Stroke l: Introduction

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.

Secondary Spinal Cord Injury llI: Pathophysiology

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

You might also read

Related Articles

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

Sort by

Same author

Diagnosis of Multiple Sclerosis Using Multimodal Deep Learning Integrating Lesion and Normal-Appearing White Matter: A Retrospective Study with International Multicentre External Validation.

medRxiv : the preprint server for health sciences·2026

Same author

Advanced brain MRI may help understand the link between migraine and multiple sclerosis.

The journal of headache and pain·2023

Same author

CADASIL mutations sensitize the brain to ischemia via spreading depolarizations and abnormal extracellular potassium homeostasis.

The Journal of clinical investigation·2022

Same author

Cutaneous Findings of Sporadic, Adult-Onset Neuronal Intranuclear Inclusion Disease.

The American Journal of dermatopathology·2021

Same author

White Matter Lesions in Migraine.

The American journal of pathology·2021

Same author

Neuronal plumes initiate spreading depolarization, the electrophysiologic event driving migraine and stroke.

Neuron·2021

Search research articles

Related Experiment Video

Updated: Apr 28, 2026

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Published on: October 4, 2024

Spreading depolarization may link migraine and stroke.

Katharina Eikermann-Haerter¹

¹Neurovascular Research Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, USA.

|June 11, 2014

Summary

Migraine significantly elevates stroke risk, especially in young adults. Suppressing spreading depolarization, a key migraine mechanism, may prevent both stroke and migraine attacks.

Keywords:

aura cerebral autosomal arteriopathy with subcortical infarcts and leukoencephalopathy familial hemiplegic migraine migraine spreading depolarization stroke

More Related Videos

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Published on: June 13, 2011

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

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

Published on: June 2, 2014

Related Experiment Videos

Last Updated: Apr 28, 2026

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice

Published on: October 4, 2024

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Modeling Neural Immune Signaling of Episodic and Chronic Migraine Using Spreading Depression In Vitro

Published on: June 13, 2011

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

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

Published on: June 2, 2014

Area of Science:

Neurology
Vascular Neurology
Neuroscience

Background:

Migraine is a prevalent neurological condition comparable to stroke risk factors like diabetes and hypertension.
Established associations link migraine and stroke through shared factors (e.g., vasculopathies, PFO) and overlapping clinical presentations (e.g., arterial dissection, migrainous stroke).

Purpose of the Study:

To investigate the underlying mechanisms connecting migraine and stroke.
To explore the role of cerebral hyperexcitability and spreading depolarization in the migraine-stroke association.
To evaluate the therapeutic potential of inhibiting spreading depolarization.

Main Methods:

Review of existing literature on migraine-stroke associations.
Experimental studies using mouse models with human migraine mutations.
Assessment of susceptibility to spreading depolarization and cerebral ischemia in mutant mice.
Evaluation of stroke phenotype prevention by suppressing spreading depolarization.

Main Results:

Migraine shares common risk factors and presentations with stroke.
Cerebral hyperexcitability and spreading depolarization are implicated in the migraine-stroke link.
Migraine mutant mice show increased susceptibility to spreading depolarization and ischemia.
Inhibiting spreading depolarization prevented stroke in these mice.

Conclusions:

Spreading depolarization is a potential mechanistic link between migraine and stroke.
Targeting spreading depolarization may offer a dual therapeutic strategy for migraine and stroke prevention.
Further clinical validation is needed to confirm these findings in human patients.