Left insular stroke is associated with adverse cardiac outcome.

BACKGROUND: After stroke, 10% of patients have adverse cardiac outcomes. Left insular damage may contribute to this by impairing sympathovagal balance (associated with cardiac structural damage and arrhythmias). METHODS: The authors conducted a prospective study of 32 patients with left insular stroke (Group 1) and 84 patients with non-insular stroke/TIA (Group 2). Adverse cardiac outcomes (cardiac death, myocardial infarction, angina, and heart failure) were assessed over 1 year. Myocardial wall motion was investigated with transesophageal echocardiography. RESULTS: Group 1's cardiac outcome relative risk (RR) compared with Group 2 was 1.75 (95% CI: 1.02, 3.00, p = 0.05). Left insular stroke remained an independent predictor of cardiac outcome in multivariate analyses. Sensitivity analysis excluding TIA and angina showed similar results. For Group 1 patients without symptomatic coronary artery disease (SCAD), cardiac outcome RR = 4.06 (95% CI: 1.83, 9.01, p = 0.002). For Group 1 with SCAD, RR = 0.36 (95% CI: 0.06, 2.13, p = 0.14). Cardiac wall motion impairment was also associated with left insular stroke independent of CAD or nonischemic heart disease. Right insular stroke was not associated with adverse cardiac outcomes or cardiac wall motion impairment. CONCLUSIONS: Left insular stroke is associated with an increased risk of adverse cardiac outcome and decreased cardiac wall motion compared to stroke in other locations and TIA. This was particularly marked in patients without symptomatic coronary artery disease (SCAD). In patients with SCAD, the cardioprotective effect of medications, especially beta-blockers alone or combined with ischemic preconditioning, may explain the lack of association in this subgroup.

Brief antiepileptic drug withdrawal prolongs interval to next seizure.

OBJECTIVE: To evaluate the course of seizure control after reinstitution of antiepileptic drugs (AEDs) in patients whose AEDs were discontinued during inpatient EEG-video monitoring. METHODS: The authors studied prospectively patients with intractable epilepsy admitted for EEG-video monitoring with AED withdrawal. They examined seizure diaries in the 2 months preceding admission and recorded the number of seizures during hospitalization and for 2 months after discharge. They also recorded the interval between the last two seizures preceding admission (S-S pre), from the last seizure to admission (S-A), from discharge to the first seizure after discharge (D-S), and between the first and the second seizures following discharge (S-S post). RESULTS: Sixty patients qualified for the study. There was a significant decrease in seizure frequency in the 2 months after discharge compared with baseline (p = 0.02). For patients who had at least two seizures during follow-up, the mean D-S interval was significantly longer than mean S-S pre and S-S post (p < 0.005), whereas the latter two intervals were comparable. Prolongation of D-S was related to duration off AEDs and to the AED restarted, but not to the number or severity of seizures during monitoring. CONCLUSION: Seizure improvement after reinstitution of antiepileptic drugs (AEDs) is due primarily to prolongation of the interval from reinstitution of AEDs to the next seizure. This may reflect increased patient responsiveness to AED therapy after a drug "holiday" and has implications for experimental AED testing in the setting of presurgical evaluation.