OBJECTIVE Hypoxia induces angiogenesis and plays a major role in the progression of carotid plaques. During carotid intervention, plaques with high-intensity signals on time-of-flight (TOF) magnetic resonance angiography (MRA) often cause ischemic stroke and embolic complications. However, the role of intraplaque hypoxia before carotid endarterectomy (CEA) and carotid artery stenting is not presently understood. In this study the authors aimed to investigate the relationship between intraplaque hypoxia and MRA findings. METHODS Nineteen consecutive patients with 20 carotid artery stenoses who underwent CEA at Saga University Hospital between August 2008 and December 2014 were enrolled in the study. The expressions of hypoxia-inducible transcription factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) were analyzed by immunohistochemical analysis. In addition, the relationship between the findings on TOF MRA and pathology for the carotid plaques was analyzed. RESULTS High-intensity plaques on TOF MRA showed higher expression levels of HIF-1α (p = 0.015) and VEGF (p = 0.007) compared with isointensity plaques. The rate of intraplaque hemorrhage (IPH) on TOF MRA was also significantly higher in the high-intensity plaques than in the isointensity plaques (p = 0.024). Finally, the mean number of neovessels was significantly higher in those without plaque hemorrhage than in those with plaque hemorrhage (p = 0.010). CONCLUSIONS Plaques with high-intensity signals on TOF MRA were associated with IPH and evidence of intraplaque hypoxia. This fact may represent an opportunity to establish novel therapeutic agents targeting intraplaque hypoxia.

Background and purposeCT scans often reveal post-interventional cerebral hyperdensities (PCHDs) immediately after intra-arterial thrombectomy (IAT) for ischemic stroke. Dual energy CT (DE-CT) can indicate whether PCHDs are caused by hemorrhage or iodinated contrast. Hyperdense lesions, detected on DE-CT with the use of iodinated contrast, could be associated with delayed hemorrhagic transformation and poor outcome. However, the quantitative indicators in DE-CT for predicting delayed hemorrhagic transformation remain unclear. We assessed such indicators for predicting delayed hemorrhagic transformation.Material and methodsWe retrospectively analyzed 52 consecutive acute ischemic stroke patients who underwent IAT. Simulated conventional CT (sCCT) images were obtained immediately after a DE-CT scan. Virtual, unenhanced, non-contrast (VNC) imaging was performed after reconstruction. Hounsfield units (HU) of the infarct areas observed on the sCCT were measured. The association of HU on sCCT with hemorrhage on VNC and delayed parenchymal hemorrhage (PH) was evaluated.ResultsThe HU of sCCT with hemorrhage on VNC was significantly higher than without it (377.9±385 HU vs 83.5±37.9 HU; P<0.0001). The cut-off index was 80 HU, which displayed 100% sensitivity, 63.8% specificity, 22.3% positive predictive value, and 100% negative predictive value (P=0.0001, area under the curve (AUC)=0.89). The HU with delayed PH was substantially higher than without it (250.8±382.2 HU vs 93.7±64.8 HU; P=0.01). The cut-off index was 78 HU, which showed 100% sensitivity, 61% specificity, 25% positive predictive value, and 100% negative predictive value (P=0.049, AUC=0.76).ConclusionsCCT images on DE-CT are useful for excluding intracerebral hemorrhage and delayed PH.

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BackgroundDopamine agonists are the standard first-line medical therapy for prolactinoma. We report a rare case of giant prolactinoma with a first epileptic seizure due to rapid reduction of the tumor as a complication of dopamine agonist therapy.Case presentationA 27-year-old Japanese man presented to our institution with a history of visual disturbance for 1 year and general fatigue for 3 months. Magnetic resonance imaging showed a tumor that arose from the pituitary and extended to the bilateral anterior skull base, the clivus, and the cavernous sinus, with compression of the optic chiasm and the bilateral frontal and temporal lobes. On the basis of the patient’s serum concentration of prolactin, we diagnosed a prolactinoma and started dopamine agonist therapy with cabergoline. The patient had a general seizure immediately after starting dopamine agonist therapy and required general anesthetic treatment following the rapid reduction of the tumor. We speculated that the rapid reduction of the tumor resulted in the retraction of the surrounding brain structure, and the epileptic seizure was then induced by dopamine agonist therapy.ConclusionsWe report a rare case of giant prolactinoma with a first epileptic seizure immediately after the initiation of dopamine agonist therapy. Clinicians need to be aware that the rapid reduction of a giant prolactinoma by dopamine agonist therapy may cause an epileptic seizure.

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