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Published on: December 16, 2021
Stroke MRI in intracerebral hemorrhage: is there a perihemorrhagic penumbra?
Peter D Schellinger1, Jochen B Fiebach, Katrin Hoffmann
1Department of Neurology, University of Heidelberg, Heidelberg, Germany. Peter_Schellinger@med.uni-heidelberg.de
Background And Purpose:
Cerebral ischemia has been proposed as a contributing mechanism to secondary neuronal injury after intracerebral hemorrhage (ICH). The search for surrogate parameters that allow treatment stratification for spontaneous ICH continues. We sought to assess the presence and prognostic effect of perihemorrhagic ischemic changes and hypoperfusion in a prospective stroke MRI study.
Methods:
We performed stroke MRI in 32 patients with hyperacute ICH (mean, 16.9+/-17.2 mL) within 6 hours after symptom onset (mean, 3.1+/-1.3 hours). Clinical data at baseline (National Institutes of Health Stroke Scale) and on day 90 (Barthel Index, modified Rankin Scale) were assessed. Perihemorrhagic perfusion- and diffusion-weighted imaging changes were assessed in a 1-cm-wide area around the clot.
Results:
Despite a mild perihemorrhagic mean transit time prolongation of 0.7+/-1.1 second, there were no significant perihemorrhagic apparent diffusion coefficient or mean transit time changes indicating irreversible ischemia or hypoperfusion. ICH size, time to imaging, or clinical severity at baseline or outcome were not reflected by changes of relative apparent diffusion coefficient or perfusion-weighted imaging. ICH size correlated with baseline clinical severity (r=0.51, P=0.005). There was a significant association (P=0.0494) and a significant negative correlation (r=-0.468, P=0.0103) of perihemorrhagic perfusion change with time from symptom onset not associated with ICH size.
Conclusions:
Perihemorrhagic hypoperfusion probably is a consequence of reduced metabolic demand (diaschisis) rather than a sign of ischemia. We found no evidence for a perihemorrhagic and potentially salvageable ischemic penumbra in hyperacute ICH. Further studies should address metabolic, toxic, apoptotic, and microvascular aspects.
Insights
This study found no evidence of salvageable ischemic penumbra around brain hemorrhages. Perihemorrhagic hypoperfusion appears to be due to reduced metabolic demand, not ischemia, in acute intracerebral hemorrhage (ICH).
Area of Science:
- Neurology
- Radiology
- Stroke Research
Background:
- Secondary neuronal injury after intracerebral hemorrhage (ICH) may involve cerebral ischemia.
- Identifying surrogate parameters for treatment stratification in spontaneous ICH is ongoing.
- The prognostic impact of perihemorrhagic ischemic changes and hypoperfusion requires further investigation.
Purpose of the Study:
- To assess the presence and prognostic significance of perihemorrhagic ischemic changes and hypoperfusion in patients with hyperacute ICH.
- To investigate potential salvageable tissue around the hemorrhage using advanced MRI techniques.
Main Methods:
- Prospective stroke MRI study involving 32 patients with hyperacute ICH within 6 hours of symptom onset.
- Assessment of perihemorrhagic perfusion-weighted imaging and diffusion-weighted imaging changes within a 1-cm area around the clot.
- Clinical data including National Institutes of Health Stroke Scale, Barthel Index, and modified Rankin Scale were collected.
Main Results:
- No significant perihemorrhagic apparent diffusion coefficient or mean transit time changes indicating irreversible ischemia were observed.
- Mild perihemorrhagic mean transit time prolongation was noted but did not correlate with ICH size or clinical severity.
- Perihemorrhagic perfusion changes showed a significant association and negative correlation with time from symptom onset, independent of ICH size.
Conclusions:
- Perihemorrhagic hypoperfusion in acute ICH is likely a consequence of diaschisis (reduced metabolic demand) rather than ischemia.
- No evidence of a salvageable perihemorrhagic ischemic penumbra was found in hyperacute ICH.
- Future research should explore metabolic, toxic, apoptotic, and microvascular factors in ICH.
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