RESUMEN
Post-stroke depression is one of the main causes of cerebrovascular and cardiovascular diseases. The aim of the present study was to investigate the efficacy of citalopram on stroke recurrence. A 52-week, randomized, double-blind, studyinvolved 440 ischemic stroke patients with depression. Patients with depression who met depression criteria of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV and V) and Hamilton Depression Rating Scale ≥ 8 (HAM-DRS) were dichotomized into patients receiving citalopram (225 patients), titrated according to clinical response, and patients with placebo (215 patients) for 52 weeks. The primary outcome measure was stroke recurrence and the secondary outcome measures were cardiovascular events and mortality. Stroke recurrence (66% vs 34%; P = 0.001) and cardiovascular events (76% vs. 24%; P = o.oo1) were significantly higher in the placebo group compared to those treated with citalopram. Multivariable analysis showed that hypertension, atrial fibrillation, and large-artery disease were significantly associated with stroke recurrence. Executive processing disorder was more associated with stroke recurrence than other neuropsychological disorders (OR, 1.74; CI95%, 1.04-2.89; P = 0.035). Survival analysis showed that treatment for depression interacted with time to reduce stroke recurrence by nearly half (39% vs. 61%; P = 0.05). The current study supports the importance of depression treatment in protecting the patients from recurrent strokes. This result warrants further studies to demonstrate the efficacy of depression treatment on stroke recurrence.
Asunto(s)
Citalopram , Accidente Cerebrovascular , Citalopram/uso terapéutico , Método Doble Ciego , Humanos , Inhibidores Selectivos de la Recaptación de Serotonina/uso terapéutico , Accidente Cerebrovascular/complicaciones , Accidente Cerebrovascular/tratamiento farmacológico , Resultado del TratamientoRESUMEN
INTRODUCTION: An evolving literature suggests a volume reduction and a loss of functional integrity of prefrontal cortex in depressed patients. Interhemispheric prefrontal functional integrity is mediated via the anterior portion of the corpus callosum. Until recently interhemispheric fibers connecting prefrontal cortex have not been well defined. In this study, we compared the corpus callosum area of depressed patients with controls using a novel schema proposed by Hofer and Frahm (2006) which defined a specific anterior callosal area for prefrontal interhemispheric fibers. We further investigated the correlation between callosal area and prefrontal cortical volume. METHODS: Thirty-six patients with major depressive disorder and thirty-three healthy controls were recruited. All subjects were psychotropic medication-free and right-handed. The imaging was performed on a 1.5T MR unit (Magnetom Vision Siemens). The images obtained from 3D MP-RAGE sequence were used for analyses. Medical Image Processing, Analyzing and Visualization (MIPAV) software was used for callosal and prefrontal measurements. RESULTS: Depressed patients had reduced prefrontal cortical volume and a loss of the normal callosal/gray matter correlation, but normal white matter volume and normal callosal areas. LIMITATIONS: It is not known if the observed changes were preexisting or acquired. CONCLUSION: Our results indicate that the normal structural relationship between anterior callosal area and prefrontal cortical volume is disrupted in major depressive disorder and that the disruption is due to reduced cortical volume rather than to changes in interhemispheric connections.