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Related Concept Videos

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...
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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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
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...
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...

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Lacunar stroke is associated with diffuse blood-brain barrier dysfunction.

Joanna M Wardlaw1, Fergus Doubal, Paul Armitage

  • 1University of Edinburgh, United Kingdom. joanna.wardlaw@ed.ac.uk

Annals of Neurology
|March 5, 2009
PubMed
Summary
This summary is machine-generated.

Patients with lacunar stroke show subtle blood-brain barrier (BBB) dysfunction in white matter, suggesting a broader issue than just ischemia. This BBB leakiness may contribute to brain abnormalities in lacunar stroke.

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Area of Science:

  • Neurology
  • Cerebrovascular Disease
  • Neuroimaging

Background:

  • Lacunar stroke, a common type of ischemic stroke (25%), is primarily attributed to intrinsic cerebral microvascular disease.
  • While ischemia is the main focus, blood-brain barrier (BBB) dysfunction or leakiness may also contribute to vessel and tissue damage.
  • The exact cause of lacunar stroke's microvascular disease remains largely unknown.

Purpose of the Study:

  • To investigate subtle, generalized blood-brain barrier (BBB) leakiness in patients diagnosed with lacunar stroke.
  • To compare BBB integrity between patients with lacunar stroke and those with cortical ischemic stroke.
  • To identify potential associations between BBB dysfunction and clinical variables in stroke patients.

Main Methods:

  • Magnetic resonance imaging (MRI) with and without intravenous gadolinium contrast was used to assess BBB leak.
  • Tissue enhancement was measured in gray matter, white matter, and cerebrospinal fluid at least one month post-stroke.
  • Two image analysis approaches (regions of interest and tissue segmentation) were employed, and general linear modeling was used for comparisons.

Main Results:

  • Signal enhancement, indicating BBB leak, was significantly higher in the white matter and cerebrospinal fluid of lacunar stroke patients compared to cortical stroke patients (p < 0.001 and p < 0.003, respectively).
  • These findings were consistent across both image analysis methods and independent of other clinical variables.
  • Increased BBB enhancement correlated with older age and enlarged perivascular spaces, but did not account for the difference between lacunar and cortical stroke groups.

Conclusions:

  • Patients experiencing lacunar stroke exhibit subtle, diffuse blood-brain barrier (BBB) dysfunction, particularly in white matter.
  • This BBB dysfunction may play a significant role in the pathophysiology of lacunar stroke.
  • Further research is needed to elucidate the interplay between BBB dysfunction and ischemia in causing the observed abnormalities in lacunar stroke.