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Related Concept Videos

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...
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...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...
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...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

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...

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Related Experiment Video

Updated: May 14, 2026

The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects
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Delayed Presentation of Subdural Hematoma.

J D Root, B D Jordan, R D Zimmerman

    The Physician and Sportsmedicine
    |July 23, 2016
    PubMed
    Summary
    This summary is machine-generated.

    Delayed subdural hematomas can occur after head injuries, even without initial loss of consciousness. Acute bleeding into chronic subdural hematomas may explain these late-onset symptoms in skiing accidents.

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    Area of Science:

    • Neurotrauma
    • Neurosurgery
    • Radiology

    Background:

    • Subdural hematomas (SDHs) are collections of blood between the dura mater and arachnoid mater.
    • Traumatic brain injuries, including those from skiing, can lead to SDHs.
    • Delayed symptom onset after head trauma is not uncommon but requires careful evaluation.

    Purpose of the Study:

    • To report two cases of delayed subdural hematomas following head injuries from skiing.
    • To highlight the potential for acute hemorrhage into chronic subdural hematomas as a cause of delayed symptoms.
    • To emphasize the importance of neuroimaging in diagnosing delayed presentations of subdural hematomas.

    Main Methods:

    • Case report of a 72-year-old man and a 47-year-old woman with subdural hematomas.
    • Review of patient history detailing repeated head injuries during skiing and subsequent symptom development.
    • Diagnostic imaging including computed tomography (CT) scan and magnetic resonance imaging (MRI) to identify hematomas.

    Main Results:

    • Both patients presented with subdural hematomas more than a month after skiing-related head injuries, without initial loss of consciousness.
    • The male patient developed a bifrontal headache after 3 asymptomatic weeks, diagnosed via CT scan.
    • The female patient experienced intermittent neurological symptoms for 4.5 months before bilateral hematomas were detected by MRI.

    Conclusions:

    • Acute hemorrhage into a pre-existing chronic subdural hematoma is a plausible explanation for the delayed symptom onset in these cases.
    • Subdural hematomas should be considered in the differential diagnosis of patients with delayed neurological symptoms after head trauma, even without a clear history of concussion.
    • Advanced neuroimaging techniques are crucial for the accurate diagnosis and management of complex subdural hematoma presentations.