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Related Experiment Video

Updated: May 28, 2026

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

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

Published on: June 18, 2021

Inflammation as a Key Driver for Chronic Subdural Hematomas.

Jane Khalife^1,2, Manisha Koneru¹, Ajith J Thomas^1,2

¹Cooper Neurological Institute, Cooper University Health Care, Camden, NJ (J.K., M.K., A.J.T.).

|May 27, 2026

Summary

This summary is machine-generated.

Chronic subdural hematomas (cSDHs) are increasingly common, particularly in the elderly. This review explores the inflammatory processes driving cSDH development and recurrence, suggesting new therapeutic targets beyond current surgical options.

Keywords:

anti-inflammatory agents cerebrovascular disorders hematoma, subdural, chronic inflammation stroke

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

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

Published on: June 10, 2020

Area of Science:

Neurosurgery
Inflammation Biology
Translational Medicine

Background:

Chronic subdural hematomas (cSDHs) incidence is rising, especially in older adults, and are projected to become the most common neurosurgical condition.
Current surgical treatments for cSDHs have high recurrence rates and often fail to address the underlying inflammatory pathology.
cSDHs involve a self-perpetuating inflammatory cycle driven by trauma, neoangiogenesis, and rebleeding.

Purpose of the Study:

To review the inflammatory mechanisms implicated in the development and progression of chronic subdural hematomas.
To highlight key biomarkers and cellular pathways involved in cSDH pathogenesis.
To discuss the translational clinical implications and potential future therapeutic targets for cSDHs.

Main Methods:

Literature review focusing on inflammatory processes in cSDHs.
Analysis of key biomarkers and cellular pathways.
Discussion of current treatment limitations and future therapeutic avenues.

Main Results:

Inflammation, neoangiogenesis, and rebleeding are central to cSDH development and recurrence.
Specific inflammatory biomarkers and cellular pathways are identified as critical drivers.
Existing treatments do not effectively target these core inflammatory mechanisms.

Conclusions:

Understanding the inflammatory cascade in cSDHs is crucial for developing more effective treatments.
Targeting inflammatory pathways offers promising opportunities to reduce cSDH recurrence.
Further research into these pathways could lead to novel therapeutic strategies for this growing neurosurgical condition.