Persistent isolated mydriasis as an early sign of internal carotid artery dissection: Pourfour du petit syndrome.

BACKGROUND: The dissection of the internal carotid artery (ICA) is commonly associated with miosis in Bernard-Horner syndrome (BHS). The presence of mydriasis is exceptional but can occur in the context of Pourfour du Petit syndrome (PDPS), a rare entity opposite of BHS accompanied by eyelid retraction and hyperhidrosis and caused by hyperactivity of the sympathetic cervical chain. AIM: To report on a case of PDPS as the first manifestation of an ICA dissection. METHOD: A 54-year-old man presented with isolated left mydriasis with no other abnormalities in the examination. Six months later, he suffered an ischemic stroke in the left middle cerebral artery territory secondary to a left ICA dissection. RESULTS: The initial study with Intracranial computed tomographic angiography and brain magnetic resonance imaging ruled out compressive cause of the third cranial nerve or structural lesion in the midbrain. The absence of hypersensitivity to Pilocarpine discarded postganglionic parasympathetic involvement. CONCLUSIONS: In the presence of unilateral mydriasis and once common causes are ruled out an imaging examination of the supra-aortic trunks should be completed, since it could represent the first sign of carotid pathology in the context of PDPS.

Utilidad del tratamiento con atorvastatina 40 mg más ezetimiba 10 mg frente a atorvastatina 80 mg en la reducción de los niveles de colesterol LDL en pacientes con ictus isquémico o ataque isquémico transitorio / Utility of treatment with atorvastatin 40 mg plus ezetimibe 10 mg versus atorvastatin 80 mg in reducing the levels of LDL cholesterol in patients with ischaemic stroke or transient ischaemic attack

Introducción. Tras un ictus isquémico, reducir los niveles de colesterol LDL (LDLc) disminuye el riesgo de recurrencia. El riesgo de recurrencia es menor con reducciones más intensas de las cifras de LDLc. Objetivo. Evaluar la eficacia y seguridad del tratamiento hipolipemiante combinado con atorvastatina 40 mg más ezetimiba 10 mg tras un ictus isquémico o ataque isquémico transitorio (AIT). Pacientes y métodos. Evaluación de la eficacia del tratamiento con atorvastatina 40 mg más ezetimiba 10 mg (n = 34) frente a atorvastatina 80 mg (n = 52) en la modificación de parámetros lipídicos tras un ictus isquémico o AIT. Se estableció como objetivo primario la obtención de niveles de LDLc ≤ 70 mg/dL o la reducción de las cifras de LDLc ≥ 50%. Adicionalmente se evaluó la presencia de efectos secundarios en ambos grupos. Resultados. Se observó un incremento significativo de las probabilidades de alcanzar el objetivo primario en el grupo tratado con atorvastatina 40 mg más ezetimiba 10 mg (odds ratio: 11,94; intervalo de confianza al 95%: 2,82-50,64; p = 0,001) y en los varones (odds ratio: 4,76; intervalo de confianza al 95%: 1,35-16,67; p = 0,02). El tratamiento con atorvastatina 40 mg más ezetimiba 10 mg obtuvo reducciones superiores de LDLc (p < 0,001), colesterol total (p = 0,001) y no HDLc (p < 0,001). Ambos tratamientos fueron seguros, con escaso número de efectos secundarios. Conclusiones. En comparación con atorvastatina 80 mg, el tratamiento con atorvastatina 40 mg más ezetimiba 10 mg incrementa la probabilidad de alcanzar los objetivos de LDLc. Ambos tratamientos son seguros y bien tolerados (AU)

Introduction. After an ischaemic stroke, to reduce LDL cholesterol (LDLc) levels decreases the risk of recurrence. The risk of recurrence is lower with more intense reductions in LDLc levels. Aim. To evaluate the efficacy and security of atorvastatin 40 mg plus ezetimibe 10 mg after ischaemic stroke or transient ischaemic attack (TIA). Patients and methods. We retrospectively evaluated stroke or TIA patients admitted to our hospital who received atorvastatin 40 mg plus ezetimibe 10 mg (n = 34) or atorvastatin 80 mg (n = 52) at discharge. We analyzed changes in lipid parameters and established as a primary outcome LDLc ≤ 70 mg/dL and/or reduction in LDLc ≥ 50%. Furthermore, safety parameters were assessed. Results. Predictors associated with primary outcome achievement were treatment with atorvastatin 40 mg plus ezetimibe 10 mg (odds ratio: 11.94; 95% CI: 2.82-50.64; p = 0.001) and male (odds ratio: 4.76; 95% CI: 1.35-16.67; p = 0.02). Treatment with atorvastatin 40 mg plus ezetimibe 10 mg achieved significantly greater reductions in LDLc (p < 0.001), total cholesterol (p < 0.001) and non-HDLc (p < 0.001). Both treatments were safe and well tolerated, with a low number of secondary effects. Conclusions. Compared with atorvastatin 80 mg, atorvastatin 40 mg plus ezetimibe 10 mg increases the likelihood of achieving LDLc goals after ischaemic stroke or transient ischaemic attack. Both treatments were safe and well tolerated (AU)

[Utility of treatment with atorvastatin 40 mg plus ezetimibe 10 mg versus atorvastatin 80 mg in reducing the levels of LDL cholesterol in patients with ischaemic stroke or transient ischaemic attack]. / Utilidad del tratamiento con atorvastatina 40 mg más ezetimiba 10 mg frente a atorvastatina 80 mg en la reducción de los niveles de colesterol LDL en pacientes con ictus isquémico o ataque isquémico transitorio.

INTRODUCTION: After an ischaemic stroke, to reduce LDL cholesterol (LDLc) levels decreases the risk of recurrence. The risk of recurrence is lower with more intense reductions in LDLc levels. AIM: To evaluate the efficacy and security of atorvastatin 40 mg plus ezetimibe 10 mg after ischaemic stroke or transient ischaemic attack (TIA). PATIENTS AND METHODS: We retrospectively evaluated stroke or TIA patients admitted to our hospital who received atorvastatin 40 mg plus ezetimibe 10 mg (n = 34) or atorvastatin 80 mg (n = 52) at discharge. We analyzed changes in lipid parameters and established as a primary outcome LDLc <= 70 mg/dL and/or reduction in LDLc >= 50%. Furthermore, safety parameters were assessed. RESULTS: Predictors associated with primary outcome achievement were treatment with atorvastatin 40 mg plus ezetimibe 10 mg (odds ratio: 11.94; 95% CI: 2.82-50.64; p = 0.001) and male (odds ratio: 4.76; 95% CI: 1.35-16.67; p = 0.02). Treatment with atorvastatin 40 mg plus ezetimibe 10 mg achieved significantly greater reductions in LDLc (p < 0.001), total cholesterol (p < 0.001) and non-HDLc (p < 0.001). Both treatments were safe and well tolerated, with a low number of secondary effects. CONCLUSIONS: Compared with atorvastatin 80 mg, atorvastatin 40 mg plus ezetimibe 10 mg increases the likelihood of achieving LDLc goals after ischaemic stroke or transient ischaemic attack. Both treatments were safe and well tolerated.

TITLE: Utilidad del tratamiento con atorvastatina 40 mg mas ezetimiba 10 mg frente a atorvastatina 80 mg en la reduccion de los niveles de colesterol LDL en pacientes con ictus isquemico o ataque isquemico transitorio.Introduccion. Tras un ictus isquemico, reducir los niveles de colesterol LDL (LDLc) disminuye el riesgo de recurrencia. El riesgo de recurrencia es menor con reducciones mas intensas de las cifras de LDLc. Objetivo. Evaluar la eficacia y seguridad del tratamiento hipolipemiante combinado con atorvastatina 40 mg mas ezetimiba 10 mg tras un ictus isquemico o ataque isquemico transitorio (AIT). Pacientes y metodos. Evaluacion de la eficacia del tratamiento con atorvastatina 40 mg mas ezetimiba 10 mg (n = 34) frente a atorvastatina 80 mg (n = 52) en la modificacion de parametros lipidicos tras un ictus isquemico o AIT. Se establecio como objetivo primario la obtencion de niveles de LDLc <= 70 mg/dL o la reduccion de las cifras de LDLc >= 50%. Adicionalmente se evaluo la presencia de efectos secundarios en ambos grupos. Resultados. Se observo un incremento significativo de las probabilidades de alcanzar el objetivo primario en el grupo tratado con atorvastatina 40 mg mas ezetimiba 10 mg (odds ratio: 11,94; intervalo de confianza al 95%: 2,82-50,64; p = 0,001) y en los varones (odds ratio: 4,76; intervalo de confianza al 95%: 1,35-16,67; p = 0,02). El tratamiento con atorvastatina 40 mg mas ezetimiba 10 mg obtuvo reducciones superiores de LDLc (p < 0,001), colesterol total (p = 0,001) y no HDLc (p < 0,001). Ambos tratamientos fueron seguros, con escaso numero de efectos secundarios. Conclusiones. En comparacion con atorvastatina 80 mg, el tratamiento con atorvastatina 40 mg mas ezetimiba 10 mg incrementa la probabilidad de alcanzar los objetivos de LDLc. Ambos tratamientos son seguros y bien tolerados.

A -174G/C polymorphism of the interleukin-6 gene in patients with lacunar infarction.

Interleukin-6 (IL-6) is a pleiotropic cytokine that plays a central role in the pathogenesis of stroke. A base pair substitution -174G/C in the promoter region of the IL-6 gene regulates IL-6 gene expression. We compared the prevalence of this polymorphism in patients with lacunar stroke and in an age- and sex-matched cohort of asymptomatic controls. Eighty-two patients with lacunar stroke and 82 asymptomatic controls were prospectively assessed and genotyped for the -174G/C polymorphism in the promoter region of the IL-6 gene. Demographics and vascular risk factors were recorded in both groups. A brain computed tomography scan/magnetic resonance imaging confirmed the clinical diagnosis of lacunar stroke in all patients. The prevalence of CC genotype (18.3 vs. 7.3%, P=0.03), and the frequency of C allele (42.7 vs. 31.1%, P=0.03) were statistically significantly higher in patients with lacunar stroke than in asymptomatic controls. Expectedly, patients with lacunar stroke had a higher prevalence of vascular risk factors than asymptomatic controls. A logistic regression model showed that independent variables associated with lacunar stroke included history of hypertension (odds ratio (OR), 7.02; 95% confidence interval (95% CI), 3.11-15.81), diabetes (OR, 5.37; 95% CI, 1.52-8.89), hyperlipidemia (OR, 3.43; 95% CI, 1.04-11.25), smoking (OR, 5.84; 95% CI, 2.15-15.84), and CC genotype of the -174G/C IL-6 gene polymorphism (OR, 4.28; 95% CI, 1.22-15.00). These findings suggest that lacunar stroke might result from genetic susceptibility to inflammation-mediated damage in concert with atherosclerotic risk factors.

Prognostic significance of uric acid serum concentration in patients with acute ischemic stroke.

BACKGROUND AND PURPOSE: We sought to assess in 881 consecutive patients with acute ischemic stroke the clinical relevance in regard to functional outcome of the natural antioxidant uric acid measured at hospital admission. METHODS: Patients had serum uric acid (mg/dL) measured by standard procedures 18.2+/-15.5 hours from clinical onset. At hospital discharge (11.0+/-6.0 days), neurological impairment was classified as moderate/severe (Mathew score < or =75; n=304) or mild/absent (Mathew score >75; n=577). Demographics, atherosclerotic risk factors, history of organ disease, baseline neurological score, stroke subtype, infarction size, renal function, aspirin use before stroke, stroke therapy, diuretic use, and laboratory markers, including erythrocyte sedimentation rate, were analyzed in both outcome groups with the use of backward logistic regression. RESULTS: Increased uric acid values were found in men, hypertensives, alcohol drinkers, and patients with coronary, pulmonary, or renal diseases. Diabetic patients had lower uric acid levels on admission. Uric acid was directly associated with hematocrit (P=0.001), sodium (P=0.001), creatinine (P=0.001), and triglycerides (P=0.001) and inversely related with nonfasting glucose (P=0.001) levels. Neurological impairment on admission (P=0.001) and final infarction size on CT/MRI (P=0.01) were also inversely associated with uric acid. A logistic regression adjusted for confounders confirmed the following independent (odds ratio, 95% CI) good outcome predictors: age (0.97, 0.96 to 0.99), Mathew score on admission (1.14, 1.12 to 1.17), erythrocyte sedimentation rate (0.98, 0.97 to 0.99), infarction volume (0.98, 0.98 to 0.99), and uric acid (1.12, 1.00 to 1.25). CONCLUSIONS: In patients with acute ischemic stroke, there is a 12% increase in the odds of good clinical outcome for each milligram per deciliter increase of serum uric acid. This finding reinforces the relevance of oxidative damage in ischemic stroke.