Cortical Neural Damage Associated with Cerebral Hyperperfusion after Reperfusion Therapy for Acute Ischemic Stroke: 123 I-iomazenil Single-photon Emission Computed Tomography Findings

Abstract

We present an 88-year-old man with cerebral hyperperfusion (CH) after acute reperfusion ther- apy. He developed acute cerebral ischemia as a result of occluded middle cerebral artery that was subsequently recanalized with endovascular thrombectomy. I-123 N-isopropyl-p-iodoam- phetamine single-photon emission computed tomography (SPECT) after reperfusion therapy showed increased cerebral blood flow (CBF) in brain areas that exhibited no abnormal findings on magnetic resonance imaging (MRI). Follow-up MRI did not demonstrate structural brain dam- age associated with CH. However, later I-123 iomazenil SPECT imaging showed a reduction in benzodiazepine receptor binding potential (BRBP) in these areas, a finding that correlates with cortical neural damage. CH is being increasingly observed after endovascular treatment for acute stroke. However, little is known about CH when not associated with cerebral hemorrhage or infarction. The role of CH after reperfusion therapy in causing brain damage remains unclear. BRBP on I-123 iomazenil SPECT images is useful to evaluate brain neural density: a reduction in cortical BRBP indicates cortical neural damage or loss. Our findings suggest that post-reperfusion hyperperfusion induces cortical neural damage even in the absence of associated brain infarction or hemorrhage on MRI. Early postoperative SPECT is recommended to detect CH after acute reperfusion therapy. CH should be considered when the recovery from stroke is unexpectedly poor for a patient.