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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...
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...
Ischemic Stroke l: Introduction01:15

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.
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...

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Brain Infarct Segmentation and Registration on MRI or CT for Lesion-symptom Mapping
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Published on: September 25, 2019

Border-zone and watershed infarctions.

Cataldo D'Amore1, Maurizio Paciaroni

  • 1Stroke Unit and Division of Internal and Cardiovascular Medicine, University of Perugia, Santa Maria della Misericordia Hospital, Perugia, Italy. cataldo.damore@gmail.com

Frontiers of Neurology and Neuroscience
|March 2, 2012
PubMed
Summary

Border-zone (BZ) and watershed infarcts result from impaired blood flow at artery junctions. These strokes present with diverse neurological deficits depending on the affected brain region, often linked to conditions causing low blood pressure.

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Area of Science:

  • Neurology
  • Vascular Neurology
  • Cerebrovascular Disease

Background:

  • Border-zone (BZ) and watershed infarcts are cerebrovascular events occurring at the interface of major arterial territories.
  • These infarcts are primarily attributed to hemodynamic compromise but microembolic causes are also considered.
  • Precipitating factors include conditions leading to hypotension or hypovolemia, such as postural changes, exertion, and blood loss.

Purpose of the Study:

  • To delineate the clinical presentations and anatomical correlates of border-zone infarcts.
  • To understand the etiological factors contributing to border-zone infarcts.
  • To differentiate BZ infarcts from other stroke types based on clinical and radiological findings.

Main Methods:

  • Review of clinical case studies and neuroimaging findings of patients with border-zone infarcts.
  • Correlation of infarct location with specific neurological deficits.
  • Analysis of patient history for predisposing hemodynamic or embolic factors.

Main Results:

  • Anterior BZ infarcts manifest as contralateral motor deficits, aphasia, or mood disturbances.
  • Posterior BZ infarcts are characterized by visual field defects (campimetric disturbances), fluent aphasia, and hemihypoesthesia.
  • Subcortical/capsule-thalamic BZ infarcts can mimic lacunar syndromes; cerebellar and brainstem BZ infarcts present with vertigo, ataxia, or coma, respectively.

Conclusions:

  • Border-zone infarcts exhibit a wide spectrum of clinical presentations contingent upon the affected vascular territory.
  • Hemodynamic instability is a key precipitant, though microembolism cannot be ruled out.
  • Recognizing the distinct neurological syndromes associated with BZ infarcts aids in diagnosis and management.