High serum levels of leptin are associated with post-stroke depression.

BACKGROUND: Depression is a frequent mood disorder that affects around 33% of stroke patients and has been associated with both poorer outcome and increased mortality. Our aim was to test the possible association between inflammatory and neurotrophic molecular markers and the development of post-stroke depression. METHOD: We studied 134 patients with a first episode of ischemic stroke without previous history of depression or speech disorders. We screened for the existence of major depression symptoms in accordance with DSM-IV criteria and a Yesavage Geriatric Depression Scale (GDS) score >11 at discharge and 1 month after stroke. At these times, serum levels of molecular markers of inflammation [interleukin (IL)-1beta, IL-6, intracellular adhesion molecule 1 (ICAM-1), tumor necrosis factor (TNF)-alpha, leptin and high-sensitivity C-reactive protein (hs-CRP)] and neurotrophic factors [brain-derived neurotrophic factor (BDNF)] were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: Twenty-five patients (18.7%) were diagnosed as having major depression at discharge. Out of 104 patients who completed the follow-up period, 23 were depressed at 1 month (22.1%). Patients with major depression showed higher serum leptin levels at discharge [43.4 (23.4-60.2) v. 6.4 (3.7-16.8) ng/ml, p<0.001] and at 1 month after stroke [46.2 (34.0-117.7) v. 6.4 (3.4-12.2) ng/ml, p<0.001). Serum levels of leptin >20.7 ng/ml were independently associated with post-stroke depression [odds ratio (OR) 16.4, 95% confidence interval (CI) 5.2-51.5, p<0.0001]. Leptin levels were even higher in the eight patients who developed depression after discharge [114.6 (87.6-120.2) v. 7.2 (3.6-13.6) ng/ml, p<0.0001]. CONCLUSIONS: Serum leptin levels at discharge are found to be associated with post-stroke depression and may predict its development during the next month.

[Cognitive impairment associated to leukoaraiosis: its pathophysiology, clinical manifestations and treatment]. / Deterioro cognitivo asociado a la leucoaraiosis: fisiopatología, manifestaciones clínicas y tratamiento.

INTRODUCTION AND DEVELOPMENT: Leukoaraiosis is a radiological term which refers to white matter disturbances observed as a hypodensity in computed tomography and hyperintensity in T2-weighted magnetic resonance image. The most accepted theory to explain the mechanism of production of leukoaraiosis is chronic ischemia, due to a damage in penetrating arteries. It is an entity with increasing interest, since it is associated with the presence of cognitive impairment. Clinical manifestations in relation with cognitive functions range from mild affectation to dementia, affecting the processing speed and executive functions. CONCLUSIONS: It seems that the control of vascular risk factors slow the progression of leukoaraiosis and cognitive impairment, and although there are no really effective treatment, it seems that some drugs, such as acetylcholinesterase inhibitors or NMDA-receptor antagonists, exert a beneficial effect, although slight, in cognitive functions.

Deterioro cognitivo asociado a la leucoaraiosis: fisiopatología, manifestaciones clínicas y tratamiento / Cognitive impairment associated to leukoaraiosis: Its pathophysiology, clinical manifestations and treatment

Introducción y desarrollo. La leucoaraiosis es un término radiológico que hace referencia a la alteración de la sustancia blanca que se observa como hipodensidad en la tomografía computarizada o como hiperintensidades en las secuencias T2 de la resonancia magnética. La hipótesis más aceptada para explicar el mecanismo de producción de la leucoaraiosis es la isquemia crónica, por afectación de las arterias perforantes. Se trata de una entidad que está provocando un interés creciente,debido a su asociación con el deterioro cognitivo. Las manifestaciones clínicas en relación con las funciones cognitivas van desde la afectación leve hasta la aparición de la demencia, y afectan fundamentalmente a la velocidad de procesamiento y a las funciones ejecutivas. Conclusiones. Parece que el control de los factores de riesgo vascular enlentece la progresión dela leucoaraiosis y del deterioro cognitivo, y, aunque no se dispone de un tratamiento realmente eficaz, es probable que algunos fármacos, como los inhibidores de la acetilcolinesterasa o los antagonistas de los receptores NMDA, ejerzan un efecto beneficioso,aunque moderado, en el rendimiento cognitivo de los pacientes

Introduction and development. Leukoaraiosis is a radiological term which refers to white matter disturbances observed as a hypodensity in computed tomography and hyperintensity in T2-weighted magnetic resonance image. The most accepted theory to explain the mechanism of production of leukoaraiosis is chronic ischemia, due to a damage in penetrating arteries. It is an entity with increasing interest, since it is associated with the presence of cognitive impairment. Clinical manifestations in relation with cognitive functions range from mild affectation to dementia, affecting the processing speed and executive functions. Conclusions. It seems that the control of vascular risk factors slow the progression of leukoaraiosis andcognitive impairment, and although there are no really effective treatment, it seems that some drugs, such as acetylcholinesterase inhibitors or NMDA-receptor antagonists, exert a beneficial effect, although slight, in cognitive functions

Marcadores moleculares de inflamación en la depresión post-ictus / Molecular markers of inflammation in post-stroke depression

Objetivo: evaluar la respuesta inflamatoria sistémica durante la fase aguda del ictus isquémico y establecer la relación entre los niveles de Factor Neurotrófico derivado del Cerebro (BDNF), IL-6, ICAM-1, el pronóstico del ictus y la incidencia de depresión. Material y métodos: Estudio prospectivo sobre 104 pacientes con primer episodio de ictus isquémico. Se recogieron antecedentes familiares de depresión y enfermedad psiquiátrica y datos familiares. Se realizó un TAC o RNM. La depresión se evaluó en el momento del alta y al mes, siguiendo el DSM IV. De muestras de sangre se obtuvieron los niveles de IL-6 e ICAM-1, BDNF. Resultados: De 104 pacientes, 54 presentaron depresión al alta y 25 depresión mayor. La depresión se relacionó con: sexo femenino, viudedad, vivir con los hijos y edad. No se halló relación con la gravedad del ictus, el grado de afectación funcional, la localización o el volumen del infarto. Tampoco entre los marcadores estudiados y la depresión tras el ictus. Conclusión: Los pacientes que desarrollan depresión tras el ictus, presentan peor pronóstico funcional, independiente del grado de afectación neurológica y de la localización de la lesión. No establecimos asociación entre la depresión y los marcadores de inflamación (AU)

Introduction: Depresión is frequent after stroke, finding an association with inflammation. Our aim is to evaluate the relationship between inflammation in acute phase of stroke and depression. Patients and methods: We included 134 patients with first ischemic stroke, excluding previous history of depression, and aphasia. Stroke severity was evaluated by NIHSS and functional outcome by modified Rankin Scale (mRS) and Barthel Index (BI). Depression was evaluated at discharge and at 1 month by DSM-IV criteria and Yesavage Scale, Serum levels of inflammatory molecules (IL-6, ICAM 1 and high-sensitive-CRP) and BDNF were determined at discharge. Results: 40,3% of patients showed depression at discharge and 48.1% at one month. Patients with depression at one month showed poor outcome (BI 70 [90,100] vs 100 [95,100]; p=0,001; mRS 2 [1,3] vs 1 [0,2]; p=0,03). Depression at discharge was independently associated with live with offspring (OR: 7,62; CI95% [1,35, 43,09]; p=0,022), and at one month with female sex (OR:5,47; CI95% [1,45,20,67]; p=0,012) and depression at discharge (OR: 9,36; CI95% [2,46,35,59]; p=0,002). We found no relationship between the molecular markers and the depression after stroke. Conclusion: No relationship was found between inflammation in acute phase and post-troke depression (AU)