Intracranial atherosclerosis is associated with progression of neurological deficit in subcortical stroke.

BACKGROUND: Progression of neurological deficit (PND) is a frequent complication of acute subcortical ischemic stroke (SCS). The role of intracranial atherosclerosis (IAS) in PND is controversial. Our goal was to evaluate IAS on admission, as predictor of PND in SCS patients. METHODS: SCS patients were identified from our prospective database from 2004 to 2008. Clinical and laboratory data were collected from charts, and radiographic data from original radiographs. The proximal intracranial arteries were graded as patent, irregular, stenotic, or occlusion. IAS was defined as irregularity or stenosis. PND was defined as a change in the National Institutes of Health Stroke Scale >1 point. RESULTS: Two hundred and two SCS patients were identified. In 14%, PND occurred at a median of 2 days from onset. Univariate analysis by infarct location showed the following to be associated with PND: for anterior circulation infarcts (centrum semiovale/basal ganglia), M1 atherosclerosis (p = 0.042); for posterior circulation infarcts, vertebral artery atherosclerosis (p = 0.018). For both groups, we found a non-significant association with age (p = 0.2) and HbA1c levels (p = 0.095). No association was found with admission glucose levels. Multivariate analysis showed the following association with PND: for anterior circulation infarcts, M1 atherosclerosis (OR 4.7; 95% CI 1.2-18.8; p = 0.03); for pontine infarcts, vertebral artery atherosclerosis (OR 5.8; 95% CI 1.1-29.4; p = 0.033). There was an increase in PND likelihood with an increasing number of atherosclerotic vessels. DISCUSSION: In our cohort of SCS patients, PND was associated with IAS of the responsible vessels. These results suggest a role for IAS in the pathogenesis of PNF in SCS patients.

Inflammatory response to intraventricular hemorrhage: time course, magnitude and effect of t-PA.

BACKGROUND: In 45% of cases of intracerebral hemorrhage (ICH) the hematoma extends into the ventricles (IVH). Intraventricular inflammation may be one mechanism by which IVH exerts deleterious effects. Tissue plasminogen activator instillation into the ventricles (IVT) has been studied for the treatment of IVH; however, its effect on IVH-induced inflammation is unknown. The purpose of this work was to describe the inflammatory response in the CSF following IVH and compare it in patients treated or not treated with IVT. METHODS: Consecutive patients diagnosed with IVH and treated with ventriculostomy were selected from our prospective stroke registry from November 2004 to July 2007. CSF protein, glucose, and WBC (corrected for RBC number) from samples collected up to 19 days after IVH were captured. Patients with evidence of CSF infection were excluded. RESULTS: 29 patients were identified: 18 in the IVT group and 11 in the non-IVT group. The two groups were comparable in terms of stroke severity and IVH volume. A brisk cellular inflammatory reaction developed around day 2, lasted 5 days and then subsided. IVT seemed to attenuate this response. There were no differences in clinical outcomes between groups. CONCLUSIONS: IVH induces intrathecal inflammatory response that peaks at day 5. IVT appears to modify this inflammation. Further work is needed to study the relationship between the intraventricular inflammatory response and patient outcome.

The IVH score: a novel tool for estimating intraventricular hemorrhage volume: clinical and research implications.

OBJECTIVE: Intraventricular extension of intracerebral hemorrhage (IVH) is an independent predictor of poor outcome. IVH volume may be important in outcome prediction and management; however, it is difficult to measure routinely. DESIGN AND PATIENTS: We reviewed the charts and computed tomographies of a cohort of consecutive patients with IVH. The cohort was divided into two groups: index and validation by random sampling. IVH and intracerebral hemorrhage (ICH) volume were measured manually in all patients. IVH was also graded using a simple classification system termed IVH score (IVHS). Clinical outcome was determined by the modified Rankin Scale (mRS) at discharge and in-hospital death. Poor outcome was defined as mRS 4-6. MAIN RESULTS: One hundred seventy-five patients were analyzed, 92 in the index group and 83 in the validation group. Exponential regression yielded the following formula for estimating IVH volume (mL): eIVHS/5 (R = .75, p < 0.001). The IVH estimation formula was then verified in the validation group (R = .8, p < 0.001). The following correlations with mRS were obtained: IVH volume R = .305; ICH volume R = .468; total volume [TV] R = .571 (p < 0.001 for all three correlations). Partial correlation of TV with mRS controlling for ICH volume yielded R = .3 for TV (p < 0.001). Logistic regression model comparing ICH and TV association with poor outcome yielded the following: ICH odds ratio = 5.2, 95% confidence interval 2.3-11.6, p < 0.001; TV odds ratio = 41.6, 95% confidence interval 9.6-180.6, p < 0.001. Substituting TV for ICH volume in the ICH score resulted in a significant increase in the specificity from 64% to 87% for predicting mortality. CONCLUSIONS: IVHS enables clinicians to rapidly estimate IVH volume. The addition of IVH to ICH volume increases its predictive power for poor outcome and mortality significantly. IVHS and TV may be used in clinical practice and clinical trials of patients with ICH.