Related Experiment Video

Updated: Jun 4, 2026

Minimally Invasive Endoscopic Intracerebral Hemorrhage Evacuation
09:01

Minimally Invasive Endoscopic Intracerebral Hemorrhage Evacuation

Published on: October 15, 2021

Intracerebral Hemorrhage

Wendy C Ziai, Vishank A Shah

    Continuum (Minneapolis, Minn.)
    |June 3, 2026
    PubMed

    Insights

    This review covers primary and secondary prevention strategies for intracerebral hemorrhage (ICH). It highlights slower recovery in ICH survivors and the need for long-term rehabilitation and management of cognitive issues.

    Area of Science:

    • Neurology
    • Neurosurgery
    • Public Health

    Background:

    • Intracerebral hemorrhage (ICH) management requires population-based risk assessment.
    • ICH survivors face risks of recurrence and arterial ischemic events.
    • Recovery and rehabilitation after ICH are critical for long-term outcomes.

    Purpose of the Study:

    • To review primary and secondary prevention strategies for spontaneous intracerebral hemorrhage (ICH).
    • To update on recovery and rehabilitation nuances for ICH survivors.
    • To discuss holistic management approaches for ICH.

    Main Methods:

    • Literature review of primary and secondary prevention concepts for ICH.
    • Analysis of current data on ICH recurrence and ischemic event prevention.
    • Evaluation of recovery patterns and rehabilitation needs in ICH survivors.

    Main Results:

    • ICH prevention involves distinct primary and secondary goals with risk assessment.
    • ICH survivors require management balancing recurrent hemorrhage and ischemic event risks.
    • Recovery is slower than ischemic stroke, emphasizing long-term support and rehabilitation.

    Conclusions:

    • Spontaneous ICH treatment remains challenging; hematoma and edema are modifiable.
    • Individualized secondary prevention is essential, balancing risks.
    • Cognitive decline and mood disorders significantly impact quality of life post-ICH.
    Abstract

    More Related Videos

    Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model09:14

    Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

    Published on: June 18, 2021

    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...
    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...
    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...
    Increased Intracranial Pressure l: Introduction01:14

    Increased Intracranial Pressure l: Introduction

    Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
    Cerebral Edema l: Introduction01:19

    Cerebral Edema l: Introduction

    Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...