Proliferation in the human ipsilateral subventricular zone after ischemic stroke.

BACKGROUND: It is uncertain whether neurogenesis occurs in humans after stroke. We studied the morphologic changes that occurred in the subventricular zone (SVZ) in patients who died following an acute ischemic stroke. METHODS: We examined coronal brain slices from patients who died after a first-ever cerebral nonlacunar infarction in the middle cerebral artery territory. We evaluated the morphologic changes in the ipsilateral and contralateral SVZ by light and electron microscopy. Using immunochemistry with Ki-67 and PCNA, we detected cell proliferation. We used Tuj-1 for immature neurons and PSA-NCAM for migrating cells. RESULTS: The study included 7 patients with a mean age of 82 +/- 5 (mean +/- SD) years; 4 were men. They died a mean of 10 +/- 5 days after the ischemic stroke. Brain samples were obtained a mean of 4 +/- 2 hours after death. In comparison with the contralateral SVZ, the following changes were observed in the ipsilateral SVZ: an increase in the width of the gap and ribbon layers, as well as in the cell density of the ribbon layer, an enlargement of the cytoplasmic volume of astrocytes, and an increase of Ki-67-positive cells. In the ipsilateral SVZ, mitoses and cells that stained for either Tuj-1 or PSA-NCAM markers were observed more frequently than in the contralateral SVZ. CONCLUSION: We found unequivocal evidence of active cell proliferation in the ipsilateral subventricular zone following an acute ischemic stroke in our patients.

Blood pressure is not associated with haematoma enlargement in acute intracerebral haemorrhage.

BACKGROUND AND PURPOSE: We performed an observational study that compared baseline and subsequent blood pressure (BP) measurements and its association with haematoma enlargement (HE) in patients with intracerebral haemorrhage (ICH). METHODS: We prospectively studied consecutive patients with supratentorial spontaneous ICH within the first 6 h after the onset of symptoms. HE was defined as an increase >or=33% in the volume of haematoma on the CT obtained 24-48 h after the onset of symptoms as compared with the CT at admission. We recorded systolic BP (SBP), diastolic BP (DBP) and mean BP (MBP) at admission and at 6, 12, 18 and 24 h after onset; the maximum SBP, DBP and MBP during the study period; the maximum SBP and DBP within intervals; the mean of all BP readings; administration of antihypertensive agents. RESULTS: We studied 60 patients whose mean age was 72.1 +/- 11.3 years. HE was observed in 27 (45%) patients. No statistically significant differences were observed in any of the analyses that compared BP parameters between the HE and non-HE groups (two-way anova). CONCLUSIONS: In an exploratory analysis, we did not find an association between BP and HE within the first 24 h after an acute ICH.

[Transthoracic echocardiography in stroke performed by neurologist: pilot study]. / Ecocardiografía transtorácica realizada por neurólogos en patología vascular: estudio piloto.

INTRODUCTION: The aim of this study is to assess concordance between transthoracic echocardiography (TTE) performed by neurologists and cardiologists for the screening of cardioembolic sources in patients with ischemic stroke. METHODS: We examined prospectively 27 consecutive patients with ischemic stroke. A potential source of embolism in all of the patients was sought by means of a TTE study. This study was performed by one neurologist after one-month full-time training on the technique and independently by one cardiologist whose results were considered as the reference standard. Regarding the risk of cardioembolism, findings from TTE studies were considered as normal, or indicative of either moderate or high risk, according to the TOAST criteria. Agreement between the two observers on the diagnosis of cardioembolic source was analyzed with the Cohen's Kappa Test (K). A K > 0,6 was considered as good agreement. RESULTS: The 27 patients studied had a mean age of 68,7 +/- 10,2 years and 70 % were men. A cardioembolic source was detected in 9 patients by the cardiologist and 8 of these were also identified by the neurologist: in 1 patient a mitral annulus calcification was not detected in the examination performed by the neurologist. In 2 patients with poor echocardiographic window, the neurologist underestimated the left ventricular function. Diagnostic agreement between both examinations was 88,9 % (K: 0,77; p = 0,001). CONCLUSION: Compared with cardiologists, trained neurologists show a fairly high degree of accuracy in the TTE screening of patients with stroke. Those cases with poor echocardiographic window or with abnormal findings should be confirmed by the cardiologists.

Aspirin or anticoagulants in stenosis of the middle cerebral artery: A randomized trial.

BACKGROUND: We report the results of an open, randomized, multicenter trial that compared the efficacy of aspirin to oral anticoagulants (OA) for the prevention of vascular events in patients with symptomatic stenosis of the middle cerebral artery (MCA). METHODS: Participants were randomly assigned to receive 300 mg/day of aspirin or a dose of OA (target INR 2-3). The MCA stenosis was demonstrated by conventional angiography or by at least two noninvasive examinations. Patients had either transient ischemic attack or cerebral infarct (CI) attributable to the MCA stenosis within 90 days before inclusion. The primary endpoint was: nonfatal CI, nonfatal acute myocardial infarct, vascular death and major hemorrhage. The patients were followed-up for a minimum of 1 year and a maximum of 3 years. RESULTS: The study included 28 patients (14 in each treatment group); the average age was 67 +/- 9.9 years. Men constituted 68% of the patients. After a mean follow-up of 23.1 +/- 10.9 months, there were no recurrences of CI in both groups. No endpoint was reported in the aspirin group, but 2 patients in the OA group (14.3%) exhibited vascular events: 1 acute myocardial infarct and 1 intracerebral hemorrhage). However, this difference was not statistically significant (p = 0.48). CONCLUSIONS: Our study suggests that aspirin is the treatment of choice for the prevention of vascular events in patients with symptomatic MCA stenosis.

Hemostatic markers of recanalization in patients with ischemic stroke treated with rt-PA.

OBJECTIVE: To determine whether pretreatment markers of coagulation and fibrinolysis are related to recanalization and functional outcome. METHODS: The authors included patients treated with IV rt-PA with occlusion on baseline transcranial Doppler (Thrombolysis in Brain Ischemia [TIBI] criteria) in whom recanalization within 6 hours was monitored. At baseline, the authors recorded data about demographics, vascular risk factors, the NIH Stroke Scale (NIHSS) score, early CT signs, etiology, blood glucose, and time to rt-PA. The authors also measured plasmatic markers of coagulation (fibrinogen, prothrombin fragments 1 + 2, Factor XIII, Factor VII) and fibrinolysis (alpha2-antiplasmin, Plasminogen Activator Inhibitor, Functional Thrombin Activatable Fibrinolysis Inhibitor [fTAFI]). A favorable outcome was defined as a modified Rankin score < 2 at 3 months. RESULTS: The authors studied 63 patients with a mean age of 67.3 +/- 12.5 years. The median NIHSS score was 16. Patients who recanalized had lower concentrations of alpha2-antiplasmin (87.5 +/- 18% vs 96.5 +/- 12.5%, p = 0.023) and fTAFI (91.7 +/- 26.7% vs 104.4 +/- 21%, p = 0.039). A multivariant logistic regression analysis showed that the level of alpha2-antiplasmin was the only predictive variable of recanalization (OR 0.95, 95% CI 0.91, 0.99, p = 0.038), while the NIHSS score was the only predictive variable of functional outcome (OR 0.81, 95% CI 0.72, 0.92, p = 0.001). CONCLUSION: Baseline levels of alpha2-antiplasmin were predictive of recanalization but were not related to the long-term outcome in patients treated with rt-PA within the first 3 hours.

Trombo carotídeo e infarto cerebral como manifestación clínica inicial de policitemia vera / Carotid thrombus and cerebral infarction as the initial clinical manifestation of polycythemia vera

La policitemia vera (PV) puede producir infarto cerebral como complicación neurológica. Los mecanismos más aceptados son la disminución del flujo cerebral por hiperviscosidad, así como alteraciones de la función plaquetaria. Presentamos una mujer de 36 años cuya manifestación clínica inicial de PV consistió en un infarto cerebral debido a un trombo carotídeo asociado a oclusión de la arteria cerebral media y de ramas corticales de la arteria cerebral anterior, demostrado por angiografía cerebral. Este caso demuestra, pues, que la PV puede producir un ictus isquémico no sólo por fenómenos trombóticos de vaso pequeño, sino también por trombosis de la arteria carótida interna o arterias cerebrales proximales. Asimismo, revisamos el tratamiento de los trombos intraluminales en arterias sin aterosclerosis ni otra patología arterial previa. Como conclusión, los síndromes mieloproliferativos, incluida la PV, deben sospecharse en todo paciente con ictus isquémico con aumento del número de plaquetas, incluso en aquellos con causas potenciales de trombocitosis reactiva

Polycythernia vera (PV) can produce cerebral infarction. The rnechanisrns proposed by most authors are hyperviscosity-related diminished cerebral blood flow and platelet function abnormalities. We present a 36-year-old woman whose initial clinical rnanifestation of PV consisted of cerebral ischernia due to a carotid thrornbus, as well as occlusion of the rniddle cerebral artery and cortical branches of the anterior cerebral artery demonstrated by angiography. To our knowledge, this is the first published case of cerebral infarction in PV caused by a thrornbus of an extracranial artery. Therefore, PV can produce ischernic stroke due to thrornbosis not only in srnall distal arteries or arterioles but also in the carotid artery or main branches. Treatment of intraluminal thrombus in non-arteriosclerotic carotid artery is discussed. Myeloproliferative disorders, including PV, must be suspected in all stroke patients with an elevated platelet count, even in those who have potential causes of reactive thrornbocytosis

Reasons for exclusion from thrombolytic therapy following acute ischemic stroke.

Despite evidence for the efficacy of thrombolytic therapy in acute ischemic stroke, only 1 to 7% of patients receive this therapy. The authors sought to determine the reasons for exclusion from tissue plasminogen activator (tPA) in an acute setting and found avoidable causes in 18% of patients. Improvements in intrahospital coordination would increase the number of patients who might benefit from tPA treatment at the authors' center.

Prognostic value of Pulsatility Index in acute intracerebral hemorrhage.

OBJECTIVE: To investigate whether data obtained by transcranial Doppler (TCD) have prognostic value in patients with intracerebral hemorrhage (ICH). METHODS: A prospective study of patients with an acute (<12 hours from onset of symptoms) spontaneous supratentorial ICH was conducted. Mortality was assessed at 30-day follow-up. TCD parameters were obtained from both middle cerebral arteries: systolic, diastolic, and mean velocities and Pulsatility Index (PI) from the affected and unaffected hemispheres. The following variables were included in a univariate analysis: age, sex, hematoma volume, hypodense volume around the hematoma, total volume, midline shift, ventricular size, Glasgow Coma Scale score, intraventricular hemorrhage, body temperature, white cell count, blood glucose, mean blood pressure, and TCD data. A multivariate analysis was performed with variables that showed significance in the univariate analysis. Receiver-operator characteristic (ROC) curves were obtained. RESULTS: Forty-eight patients (age 66.5 +/- 12.5 years; 28 men) were studied. Mortality at 30 days was 31%. The only predictor of mortality was the Glasgow Coma Scale score (odds ratio [OR] 0.67, CI 0.53 to 0.84, p = 0.001), whereas the PI from the unaffected hemisphere was correlated with mortality (OR 2.3, CI 0.92 to 5.72, p = 0.07). The area under the ROC curve was 0.92. A cutoff for PI from the unaffected hemisphere of 1.75 showed a specificity of 94% and a sensitivity of 80% as a predictor of death at 30 days. CONCLUSIONS: The PI of the unaffected hemisphere may be a predictor of death in acute ICH. These findings suggest that intracranial hypertension is the most likely cause of death in most patients with ICH.