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Updated: Jun 14, 2026
06:01
A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Brainstem hyperperfusion syndrome after intravenous thrombolysis: a case report
Chi-Ieong Lau1, Li-Ming Lien, Wei-Hung Chen
1Department of Neurology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan.
Summary
Recombinant tissue plasminogen activator (rtPA) can cause brainstem hyperperfusion syndrome, leading to delayed neurological deterioration after acute stroke treatment. This condition, characterized by vasogenic edema, is a newly identified cause of delayed functional improvement.
Area of Science:
- Neurology
- Neuroimaging
- Vascular Medicine
Background:
- Recombinant tissue plasminogen activator (rtPA) is a key treatment for acute ischemic stroke.
- Hyperperfusion syndrome following rtPA has not been previously reported in the brainstem.
Observation:
- A 59-year-old male patient experienced delayed functional improvement (DFI) after rtPA treatment for acute ischemic stroke.
- Magnetic resonance imaging (MRI) revealed reversible pontine hyperintensity on diffusion-weighted imaging (DWI).
- Transcranial Doppler scans showed transient increases in basilar arterial flow.
Findings:
- The observed MRI and Doppler findings suggest vasogenic edema and hyperperfusion in the brainstem.
- This rtPA-associated brainstem hyperperfusion syndrome can manifest as transient neurological deficits.
- It represents a potential cause of DFI, distinct from reocclusion.
Implications:
- This study identifies rtPA-associated hyperperfusion syndrome as a novel cause of delayed neurological deterioration after stroke.
- Understanding this phenomenon is crucial for accurate diagnosis and management of post-stroke complications.
- Further research is warranted to explore the incidence and mechanisms of rtPA-induced brainstem hyperperfusion.
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