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Optimized Management of Endovascular Treatment for Acute Ischemic Stroke
Published on: January 18, 2018
Variability of the systemic acute phase response after ischemic stroke.
Craig J Smith1, Hedley C A Emsley, Andy Vail
1Division of Medicine and Neurosciences, University of Manchester, Clinical Sciences Building, Hope Hospital, Salford, UK. csmith@fs1.ho.man.ac.uk
Journal of the Neurological Sciences
|November 8, 2006
Summary
The size of brain damage after ischemic stroke significantly impacts the acute phase response (APR), a marker of inflammation. Larger infarct volumes correlate with a stronger APR, suggesting brain injury is a key driver of this systemic response.
Area of Science:
- Neuroscience
- Immunology
- Biomarkers
Background:
- Ischemic stroke is associated with the acute phase response (APR), but individual responses vary significantly.
- Understanding factors influencing APR variability is crucial for patient management and prognosis.
Purpose of the Study:
- To analyze individual acute phase response (APR) profiles in ischemic stroke patients.
- To investigate the relationship between the volume of brain infarction and the APR.
- To assess the correlation between plasma C-reactive protein (CRP) and interleukin-6 (IL-6) levels with infarct size.
Main Methods:
- Post-hoc analysis of 31 ischemic stroke patients.
- Serial blood sampling for plasma CRP and IL-6 analysis up to 12 months post-stroke.
- Computed tomography (CT) to measure brain infarct volume at 5-7 days.
Main Results:
- 94% of patients showed increased CRP by day 5-7, with a median increase of 558%.
- CRP response correlated strongly with CT infarct volume (r=0.62, p<0.001).
- Greater infarct volumes were associated with more evidence of infection.
- IL-6 response showed a similar pattern, though less consistently.
Conclusions:
- The extent of acute brain injury after ischemic stroke is a primary determinant of the magnitude and variability of the APR.
- While infection can contribute, brain infarct volume plays a major role in systemic inflammation following stroke.
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