Related Experiment Video

Updated: Aug 5, 2026

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection
08:22

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection

Published on: July 21, 2013

History of occlusive cerebrovascular disease I. from Wepfer to Moniz

E S Gurdjian, E S Gurdjian

    Archives of Neurology
    |June 1, 1979
    PubMed

    Insights

    Early descriptions of cerebrovascular disease in the 17th century linked occlusive carotid and vertebral artery disease to apoplexy. Willis identified collateral circulation as a stroke prevention mechanism.

    Area of Science:

    • Neurology
    • Vascular Medicine
    • Medical History

    Background:

    • The historical understanding of cerebrovascular disease dates back to the 17th century.
    • Early researchers investigated the causes of apoplexy (stroke).

    Observation:

    • Wepfer (1658) proposed that occlusive disease of the carotid and vertebral arteries caused apoplexy.
    • Willis (1665) described collateral blood flow pathways within the brain's vasculature.

    Findings:

    • Willis's observations suggested that these collateral channels could mitigate the effects of arterial occlusion.
    • This indicated a potential protective mechanism against stroke development.

    Implications:

    • These early findings laid the groundwork for understanding stroke pathophysiology.
    • The concept of collateral circulation remains crucial in cerebrovascular research and treatment strategies.

    More Related Videos

    Protocol for Isolating the Mouse Circle of Willis06:30

    Protocol for Isolating the Mouse Circle of Willis

    Published on: October 22, 2016

    Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations14:58

    Comprehensive Endovascular and Open Surgical Management of Cerebral Arteriovenous Malformations

    Published on: October 20, 2017

    Related Concept Videos

    Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation01:21

    Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

    Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
    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.
    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...
    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...
    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...
    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...