Identifying depression in epilepsy in a busy clinical setting is enhanced with systematic screening.

PURPOSE: Depression is a highly prevalent, relatively underdiagnosed and undertreated comorbid condition in epilepsy. The purpose of this study was to determine the effect of using a validated self-reporting depression scale on the ability to detect depression in people with epilepsy receiving care in a busy clinical setting. METHODS: The Neurological Disorders Depression Inventory for Epilepsy (NDDI-E) is a 6-item questionnaire validated to screen for depression in people with epilepsy. We performed a retrospective chart review of 192 consecutive patients who had completed the NDDI-E while receiving care at a seizure clinic in the largest public hospital in Houston, Texas. For comparison, charts of 192 consecutive patients receiving care immediately prior to the implementation of the NDDI-E in the same clinic were assessed. RESULTS: Fifty-five (28.6%) of patients screened positive for depression with the NDDI-E. They subsequently received a semi-structured psychiatric interview based on the DSM-IV model and 89% (n=49) were confirmed to have major depression. Use of the NDDI-E thus resulted in the detection of active depression in 25.5% (n=49) of the patients, whereas only 2.6% (n=5) of patients in the group not systematically screened were found to have active depression (p<0.0001). Thirty-two of the 49 (65%) patients with depression detected by screening were not previously diagnosed or treated. Multivariate analysis revealed that a history of depression, seizure frequency, and topiramate use were independent predictors of depression. Lamotrigine use was protective against depression. DISCUSSION: Use of the NDDI-E significantly improved the ability to detect depression in epilepsy patients in a busy clinical practice.

Protective effects of beta-blockers in cerebrovascular disease.

OBJECTIVE: Because activated sympathetic tone is associated with poorer outcome after stroke, we investigated whether beta-blocker treatment was associated with lesser stroke severity and improved outcome. METHOD: We prospectively studied 111 patients with stroke. Stroke severity on presentation gauged by Canadian Neurologic Scale (CanNS) and medication use verified from medical records. Power spectral analysis of heart rate variability estimated cardiac sympathovagal tone. Coagulation and inflammatory activity were assessed. RESULTS: On multiple linear regression, beta-blocker use was the sole independent predictor of less severe stroke on presentation (95% CI: 0.12 to 1.86: p = 0.03). When CanNS was dichotomized, multiple logistic regression revealed that beta-blocker use (odds ratio [OR] 3.70, 95% CI: 1.24 to 11.01, p = 0.02) and female gender (OR 2.96, 95% CI: 1.14 to 7.69, p = 0.03) were independent predictors of CanNS score >8.5. There was no difference in blood pressure and blood glucose between these two groups. Beta-blocker treatment was associated with lower sympathovagal tone (p = 0.001), thrombin (p = 0.009), hemoglobin A(1)C levels (p = 0.02), and erythrocyte sedimentation rate (p = 0.003). CONCLUSION: Beta-blocker use is associated with less severe stroke on presentation and may be cerebroprotective due to a sympatholytic effect associated with decreased thrombin, inflammation, and hemoglobin A(1)C.

Effect of estrogen plus progestin on stroke in postmenopausal women: the Women's Health Initiative: a randomized trial.

CONTEXT: The Women's Health Initiative (WHI) trial of estrogen plus progestin was stopped early because of adverse effects, including an increased risk of stroke in the estrogen plus progestin group. OBJECTIVE: To assess the effect of estrogen plus progestin on ischemic and hemorrhagic stroke and in subgroups, and to determine whether the effect of estrogen plus progestin was modified by baseline levels of blood biomarkers. DESIGN: Multicenter double-blind, placebo-controlled, randomized clinical trial involving 16 608 women aged 50 through 79 years with an average follow-up of 5.6 years. Baseline levels of blood-based markers of inflammation, thrombosis, and lipid levels were measured in the first 140 centrally confirmed stroke cases and 513 controls. INTERVENTIONS: Participants received 0.625 mg/d of conjugated equine estrogen plus 2.5 mg/d of medroxyprogesterone acetate (n = 8506) or placebo (n = 8102). MAIN OUTCOME MEASURES: Overall strokes and stroke subtype and severity were centrally adjudicated by stroke neurologists. RESULTS: One hundred fifty-one patients (1.8%) in the estrogen plus progestin and 107 (1.3%) in the placebo groups had strokes. Overall 79.8% of strokes were ischemic. For combined ischemic and hemorrhagic strokes, the intention-to-treat hazard ratio (HR) for estrogen plus progestin vs placebo was 1.31 (95% confidence interval [CI], 1.02-1.68); with adjustment for adherence, the HR was 1.50 (95% CI, 1.08-2.08). The HR for ischemic stroke was 1.44 (95% CI, 1.09-1.90) and for hemorrhagic stroke, 0.82 (95% CI, 0.43-1.56). Point estimates of the HRs indicate that excess risk of all stroke was apparent in all age groups, in all categories of baseline stroke risk, and in women with and without hypertension, prior history of cardiovascular disease, use of hormones, statins, or aspirin. Other risk factors for stroke, including smoking, blood pressure, diabetes, lower use of vitamin C supplements, blood-based biomarkers of inflammation, higher white blood cell count, and higher hematocrit levels did not modify the effect of estrogen plus progestin on stroke risk. CONCLUSIONS: Estrogen plus progestin increases the risk of ischemic stroke in generally healthy postmenopausal women. Excess risk for all strokes attributed to estrogen plus progestin appeared to be present in all subgroups of women examined.