European neurology · 2007
Development of cerebral infarction shortly after intracerebral hemorrhage.
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Kim Chul H, Kim Jong S
Аннотация
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.
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.