Related Experiment Video

Updated: Apr 22, 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

Persistent aura with small occipital cortical infarction: implications for migraine pathophysiology

Sam Thissen1, Peter J Koehler1

  • 1Department of Neurology, Atrium Medical Centre, Heerlen, The Netherlands.

Case Reports in Neurology
|October 10, 2014
PubMed
Abstract

Insights

Persistent migraine aura (PMA) with infarction, previously unreported, may support the intracortical disinhibition hypothesis. This case highlights potential links between infarction and hyperexcitability in migraine aura pathophysiology.

Area of Science:

  • Neurology
  • Neuroscience

Background:

  • Migraine with aura pathophysiology involves cortical spreading depression and hypersensitivity, potentially involving inhibitory interneurons.
  • Persistent migraine aura (PMA) is defined as aura symptoms lasting over a week without infarction.

Observation:

  • A case of persistent aura with an occipital cortical infarction was identified.
  • The patient presented with persistent aura symptoms, but imaging revealed an occipital cortical infarction with reduced metabolic activity.

Findings:

  • The infarction may have caused an imbalance in hyperexcitable visual cortex networks already affected by migraine aura.
  • This case, while not meeting PMA criteria due to infarction, exhibited persistent aura symptoms.

Implications:

  • This is the first reported case of persistent aura with occipital infarction.
  • Findings may support the intracortical disinhibition hypothesis in migraine, suggesting infarction could exacerbate aura-related network imbalances.
Keywords:
Cortical hyperexcitabilityInhibitory GABAergic network cellsIntracortical disinhibition hypothesisMigraine with auraPersistent migraine aura

More Related Videos

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection08:22

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection

Published on: July 21, 2013

14.6K
Assessing Cortical Cerebral Microinfarcts on High Resolution MR Images08:39

Assessing Cortical Cerebral Microinfarcts on High Resolution MR Images

Published on: November 20, 2015

12.8K

Related Concept Videos

Transient Ischemic Attack l: Introduction01:26

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...
4
Association Areas of the Cortex01:21

Association Areas of the Cortex

Association areas are regions of the cerebral cortex that do not have a specific sensory or motor function. Instead, they integrate and interpret information from various sources to enable higher cognitive processes such as memory, learning, and decision-making. Some key association areas include the following:
Prefrontal Association Area: This area is located in the frontal lobe and is involved in planning, decision-making, and moderating social behavior. It connects with primary motor areas,...
10.1K
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...
7
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...
4
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...
10
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...
7