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Background and Purpose— Microembolic signals (MES) found on transcranial Doppler range from harmless air bubbles to large, solid, particulate emboli from the heart and large vessels. The presence of MES is not always associated with poor clinical outcome. The purpose of our study was to determine whether the relative energy index of MES measured by power M-mode Doppler can distinguish malignant from benign MES and to identify patients with worse prognosis. Methods— We prospectively collected transcranial Doppler emboli monitoring data from patients with symptomatic carotid stenosis presenting with TIA or ischemic stroke. For each patient, we calculated the relative energy index of MES and categorized those >1.0 as malignant MES. We compared the clinical characteristics, number, and volume of diffusion-weighted imaging lesions, and degree of stenosis and plaque characteristics on CT angiogram of patients with malignant and benign MES. Results— We enrolled 92 patients, 29 with TIA and 63 with stroke, within 48 hours of symptom onset. Twenty-six patients had a total of 319 MES; of these, 82.4% were benign and were 17.6% malignant. Malignant MES traveled further within intracranial vessels than benign MES. The 9 patients with >1 malignant MES had significantly larger baseline diffusion-weighted imaging lesion volume, had a higher prevalence of intraluminal thrombus on CT angiogram of the neck and plaque ulceration, and were more likely to have a poor clinical outcome (modified Rankin Score ≥2) than those with benign MES (OR, 6.5; 95% CI, 1.47–28.68). The presence of malignant MES led to the institution of more aggressive secondary prevention measures. Conclusions— Power M-mode transcranial Doppler identifies a subgroup of patients with malignant MES. These signals are more frequent in longer arterial trajectory. Patients with malignant MES have larger baseline infarcts, a higher prevalence of intraluminal thrombus or ulcerated plaque in the carotid artery, and worse clinical outcome.

BACKGOUND: We evaluated the safety of the steps during carotid stenting. METHODS: This was a prospective single-arm study. Cases were monitored by TCD during the stenting procedure. The time of each of 11 steps was recorded and noted during TCD interpretation. Post stenting MRI was done in all patients. Emboli on TCD were classified based on the relative energy index of microemboli (REIM) method into microemboli (REIM ≤ 1) or malignant (REIM >1). Medians were compared using Mann-Whitney test. A negative binomial model was used to investigate the predictive value of TCD findings on new DWI hits. RESULTS: We enrolled 30 subjects. The median age was 70.5 years and 23.3% were asymptomatic. The median count of embolic signals was 212.5 (108 microemboli, 80 malignant). Stent deployment had the highest median count 58 (31 microemboli, 20 malignant) followed by protection device deployment 30 (21 microemboli, 10 malignant, (p value 0.0006)) “Figure”. On post stenting MRI, 80% had new DWI hits. The median DWI count was 4 (range 0-33). The median volume of DWI hits was 0.4 ml (range 0 - 6.1 ml). 63% of patients had a total volume under 1 ml. Only 2 patients (6.7%) had new deficits post stenting. The median DWI volume in those patients was 3.0 ml compared to 0.6 ml in asymptomatic cases (p 0.037). Median emboli count in those with vs. without new deficits was not different (p 0.87) Total TCD emboli count did not predict DWI hits, adjusting for age and symptoms’ status (p 0.25). Malignant emboli predicted new DWI hits (p 0.044). For every malignant embolus, the expected count of DWI hits increases by 1% (CI95 0-2%). There was no relation between total or malignant emboli with the DWI volume. CONCLUSIONS: In this prospective study, we observed a high incidence of emboli on TCD during stenting, especially when stent and protection device were deployed. Most patients developed new DWI hits but only 6.7% had new deficits. The combined DWI volume was less than 1.0 ml in most cases. Only malignant emboli predicted new DWI hits.