Related Experiment Video
Updated: May 6, 2026
10:44
Modeling Intracerebral Hemorrhage in Mice: Injection of Autologous Blood or Bacterial Collagenase
Published on: September 22, 2012
24.3K
Complement Inhibition in Chronic Subdural Hematoma Fluid
Niklas Marklund1, Shaian Zolfaghari1, Gustaf Westerberg1
1Department of Clinical Sciences Lund, Division of Neurosurgery, Department of Neurosurgery, Lund University and Skane University Hospital, Lund, Sweden.
Inflammation
|December 9, 2024
Summary
Chronic subdural hematoma (CSDH) involves altered complement system levels. Complement inhibitor Clusterin increased, while C5a and C9 decreased, suggesting impaired debris clearance and inflammation.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Chronic subdural hematoma (CSDH) pathophysiology is complex, with inflammation potentially playing a role.
- The involvement of the complement system in CSDH remains largely unknown.
- Investigating the complement system's contribution to CSDH is crucial for understanding disease mechanisms.
Purpose of the Study:
- To investigate the role of the complement system in chronic subdural hematoma (CSDH) pathophysiology.
- To analyze biomarkers of inflammation and complement activation in CSDH fluid and peripheral blood.
- To examine CSDH membranes and dura for complement component deposition.
Main Methods:
- Simultaneous collection of CSDH fluid and peripheral blood from 20 CSDH patients.
- Immunohistochemistry of CSDH capsule and dura for C5b-C9 and C5a.
- Multiplex assay for inflammation and complement biomarkers (Adiponectin, Clusterin, C9, CRP) and C5a analysis.
Main Results:
- Ten biomarkers differed significantly between CSDH fluid and peripheral blood.
- Clusterin and Cystatin C were increased in CSDH fluid; C5a, Complement 9, and Adiponectin were decreased.
- No C5a or C5b-C9 membrane attack complex immunoreactivity was found in the dura or CSDH membrane.
Conclusions:
- CSDH exhibits increased levels of complement inhibitor Clusterin and decreased levels of C5a and C9.
- The absence of membrane attack complex C5b-C9 suggests it's not a major factor in CSDH membranes.
- Complement inhibition may impair CSDH debris clearance and promote secondary inflammation.
More Related Videos
06:29Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
Published on: January 29, 2014
30.5K
09:58A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side
Published on: May 6, 2016
14.2K
Related Concept Videos
01:27Complement System
10.8K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
10.8K
01:17Hemorrhagic Stroke l: Introduction
34
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...
34
01:29Hemorrhagic Stroke ll: Pathophysiology
52
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...
52
01:19Cerebral Edema l: Introduction
34
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...
34
01:22Cerebral Edema ll: Pathophysiology
31
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...
31
01:21Cytotoxic Edema: Pathophysiology
31
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous...
31