Related Experiment Video

Updated: Jun 14, 2026

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model
05:12

Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model

Published on: September 4, 2017

11.0K

Inflammatory Mechanisms in a Neurovascular Disease: Cerebral Cavernous Malformation

Ying Li1,2, Abhinav Srinath2, Roberto J Alcazar-Felix2

  • 1Department of Neurosurgery, First Affiliated Hospital of Harbin Medical University, Harbin 150001, China.

Brain Sciences
|September 28, 2023
PubMed

Insights

Cerebral cavernous malformation (CCM) involves an inflammatory microenvironment that drives disease progression. Understanding immune responses in CCM is key for developing new diagnostic and treatment strategies.

Area of Science:

  • Neuroimmunology
  • Cerebrovascular Diseases
  • Inflammation Biology

Background:

  • Cerebral cavernous malformation (CCM) is a prevalent cerebrovascular disorder.
  • CCM lesions exhibit a distinct inflammatory microenvironment influencing disease severity.
  • Intracranial hemorrhage, seizures, and focal deficits are common clinical manifestations.

Purpose of the Study:

  • To review the inflammatory cell infiltrate within CCM lesions.
  • To explore the role of antigen-driven immune responses in CCM pathogenicity.
  • To summarize immune mechanisms in CCM pathogenesis and progression, including immunothrombosis.

Main Methods:

  • Literature review of immunological mechanisms in CCM.
  • Analysis of immune cell infiltration in CCM lesions.
  • Examination of circulating inflammatory biomarkers in CCM patients.

Main Results:

  • CCM pathogenesis is linked to specific immune responses and inflammatory microenvironments.
  • Loss of CCM gene function influences immune cell activity and disease progression.
  • Circulating inflammatory biomarkers correlate with CCM disease activity.

Conclusions:

  • Immune mechanisms are central to CCM pathogenesis and clinical course.
  • Further research into cellular contributions and biomarkers can guide therapeutic development.
  • Findings have implications for diagnosing and treating CCM and other neurovascular diseases.
Keywords:
cerebral cavernous malformationimmune responseimmunothrombosisinflammationtranscriptome

More Related Videos

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage08:12

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

Published on: July 28, 2018

8.1K
A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

1.9K

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...
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...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
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 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...
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...