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Published on: June 18, 2021
Development of cerebral infarction shortly after intracerebral hemorrhage
1Department of Neurology, Kyung Hee University, East-West Neo Medical Center, Seoul, South Korea.
Insights
Intracerebral hemorrhage (ICH) can lead to early cerebral infarction (CI) through various mechanisms. This study characterizes this rare complication and its contributing factors.
Area of Science:
- Neurology
- Neuroscience
- Vascular Neurology
Background:
- Cerebral infarction (CI) shortly after intracerebral hemorrhage (ICH) is a rare clinical event.
- Understanding the pathophysiology of CI post-ICH is crucial for patient management.
Purpose of the Study:
- To characterize the clinical presentation of early CI following ICH.
- To investigate the potential mechanisms contributing to CI development after ICH.
Main Methods:
- Retrospective analysis of 6 patients who developed CI within 10 days of ICH onset.
- Review of initial ICH locations, causes, clinical course, and follow-up imaging findings.
Main Results:
- Initial ICHs were primarily hypertensive in origin, located in the putamen, thalamus, or cerebellum.
- Patients experienced neurological worsening or symptom changes within 10 days, with imaging confirming lacunar or territorial infarcts.
- Potential contributing factors included mechanical compression, dehydration, hypotension, infection, and small-vessel disease.
Conclusions:
- ICH can predispose patients to subsequent infarcts via multiple pathways.
- Mechanisms include mechanical compression, hemodynamic instability, inflammation, and underlying small-vessel pathology.
Background And Purpose:
Cerebral infarction (CI) occurring soon after intracerebral hemorrhage (ICH) has been rarely reported. The purpose of the present study was to characterize this condition and discuss the possible pathophysiology.
Method:
We retrospectively studied 6 patients who developed CI within 10 days after the onset of ICH.
Results:
The initial ICHs were located in the putamen (n=3), thalamus (n=2) and cerebellum (n=1), and were considered to be caused by hypertension in all of the patients. They showed sudden worsening (n=4) or change in neurologic symptoms (n=2) within 10 days after the initial ICH. Follow-up imaging revealed corresponding lacunar (n=2) and territorial (n=4) infarcts. Possible factors related to the development of new CIs included mechanical compression of cerebral vessels (n=2), dehydration (n=4), hypotension (n=2), infection (n=2) and concomitant small-vessel pathology (n=2).
Conclusions:
ICH may predispose certain patients to the development of infarcts through a combination of mechanisms, including mechanical compression of cerebral vessels, hemodynamic instability, inflammation and concomitant small-vessel pathology.
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