The Effect of Pulsatility Index on Infarct Volume in Acute Lacunar Stroke.

PURPOSE: Lacunar stroke, in the context of small vessel disease, is a type of cerebral infarction caused by occlusion of a penetrating artery. Pulsatility index (PI) is an easily measurable parameter in Transcranial Doppler ultrasound (TCD) study. PI reflects distal cerebral vascular resistance and has been interpreted as a surrogate marker of small vessel disease. We hypothesized that an increased PI, a marker of small vessel disease, might be associated with a larger infarct volume in acute lacunar stroke. MATERIALS AND METHODS: This study included 64 patients with acute lacunar stroke who underwent TCD and brain MRI. We evaluated the association between the mean PI value of bilateral middle cerebral arteries and infarct volume on diffusion-weighted MRI using univariate and multivariate linear regression. RESULTS: The mean infarct volume and PI were 482.18±406.40 mm³ and 0.86±0.18, respectively. On univariate linear regression, there was a significant positive association between PI and infarct volume (p=0.001). In the multivariate model, a single standard deviation increase of PI (per 0.18) was associated with an increase of 139.05 mm³ in infarct volume (95% confidence interval, 21.25 to 256.85; p=0.022). CONCLUSION: We demonstrated that PI was an independent determinant of infarct volume in acute lacunar stroke. The PI value measured in acute stroke may be a surrogate marker of the extent of ischemic injury.

Plasma total homocysteine level is associated with the pulsatility index of cerebral arteries in lacunar infarction.

PURPOSE: The pulsatility index (PI), measured by transcranial Doppler (TCD), is a surrogate marker for distal vascular resistance in cerebral arteries, and elevated plasma total homocysteine (tHcyt) is regarded as a cause of ischemic stroke, including lacunar infarction. We investigated the relationship between the PI of cerebral arteries and plasma tHcyt in patients with lacunar infarction. MATERIALS AND METHODS: Plasma tHcyt level and TCD examination were performed in 94 patients with lacunar infarction. Mean flow velocity (MFV) and PI were assessed at the ipsilateral middle cerebral artery (MCA) and contralateral MCA, relative to the infarction, and the basilar artery (BA). Multivariate regression analysis was conducted between log-transformed tHcyt levels (logHcyt) and the PI of individual arteries. RESULTS: There was a significant correlation between logHcyt and the PI in all tested arteries (ipsilateral MCA: r=0.21, p=0.03; contralateral MCA: r=0.21, p=0.04; BA: r=0.35, p=0.01). In multivariate regression analysis, this significance remained unchanged after adjusting for vascular risk factors, creatinine, hematocrit and platelet count (ipsilateral MCA: ß=0.26, p=0.01; contralateral MCA: ß=0.21, p=0.04; BA: ß=0.39, p=0.001). There was no significant association between logHcyt and MFV of individual arteries. CONCLUSION: A significant association between plasma tHcyt and the PI of cerebral arteries indicates that homocysteine plays a role in the increase of distal arterial resistance in lacunar infarction.

Limited clinical value of multiple blood markers in the diagnosis of ischemic stroke.

OBJECTIVES: No ideal blood marker exists for the diagnosis of ischemic stroke. Combined use of multiple blood markers would enhance the ability of clinical diagnosis of ischemic stroke. DESIGN AND METHODS: Blood concentrations of neuronal markers (NSE, VSNL-1, hFABP, and Ngb), astroglial markers (S100B and GFAP), inflammatory markers (IL-6 and TNF-α), blood-brain barrier marker (MMP-9), and hemostatic markers (PAI-1) were measured within 6-24 h of stroke onset. The area under the receiver operator characteristic (AUROC) curve of patients with ischemic stroke and stroke-mimic was compared after adding individual or a combination of blood markers to the clinical diagnostic assessment (age, atrial fibrillation, and Face-Arm-Speech Test [FAST]). RESULTS: Despite acute elevations of blood IL-6, S100B, MMP-9, hFABP, and PAI-1 in univariate analysis, only IL-6, S100B, and MMP-9 were independently associated with ischemic stroke in multivariate analysis. The addition of biomarkers (IL-6, S100B, and MMP-9) did not improve the diagnostic performance of baseline clinical models with added biomarkers versus baseline clinical models alone (AUROC, 0.865 vs. 0.837, p=0.069). CONCLUSIONS: IL-6, S100B, and MMP-9 markers are elevated in the peripheral blood during the acute phase of ischemic stroke. However, the clinical usefulness of these biomarkers is limited due to low discriminating ability when compared to clinical parameters alone in diagnosis of ischemic stroke.

Abdominal wall hemorrhage after intravenous thrombolysis for acute ischemic stroke.

BACKGROUND: Thrombolysis is strongly recommended for patients with significant neurologic deficits secondary to acute ischemic stroke. Extracranial bleeding is a rare but major complication of thrombolysis. CASE PRESENTATION: A 78-year-old woman presented with acute ischemic stroke caused by occlusion of the basilar artery. Clinical recovery was observed after successful recanalization by intravenous thrombolysis and intraarterial thrombectomy. However, the patient complained of sudden abdominal pain following the intervention and a newly developed abdominal wall mass was found. CT scan and selective angiography confirmed active bleeding from the left epigastric artery into the abdominal muscle layer and the bleeding was successfully managed by selective embolization of the bleeding artery. CONCLUSIONS: We report a rare case of abdominal wall hemorrhage after thrombolysis for acute ischemic stroke. The findings indicate that abdominal wall hemorrhage should be considered as a differential diagnosis in the presence of abdominal discomfort after thrombolysis for acute ischemic stroke.

Different impact of hyperhomocysteinemia on cerebral small vessel ischemia and cervico-cerebral atherosclerosis in non-stroke individuals.

BACKGROUND: Our aim was to investigate the impact of plasma total homocysteine (tHcyt) levels on cervico-cerebral atherosclerosis and cerebral small vessel ischemia in non-stroke individuals. METHODS: Demographic, laboratory, brain magnetic resonance imaging and magnetic resonance angiographic data were retrospectively analyzed in 682 non-stroke individuals. The association between plasma tHcyt and radiological indices of cervico-cerebral atherosclerosis (any presence of cervico-cerebral [aCC] atherosclerosis, extracranial [EC] atherosclerosis and intracranial [IC] atherosclerosis) and cerebral small vessel ischemia (silent brain infarct [SBI] and cerebral white matter hyperintensity [cWMH]) was analyzed after adjusting for cardiovascular risk factors. RESULTS: There was no association between values for natural log-transformed tHcyt (log-Hcyt) and aCC atherosclerosis, EC atherosclerosis, or IC atherosclerosis. The log-Hcyt was independently associated with cWMH (OR: 3.07, 95% CI: 1.64-5.75) and SBI (OR: 2.91, 95% CI: 1.57-5.40) in multivariate analysis. Median plasma tHcyt level increased as the severity of cWMH increased. CONCLUSIONS: Our results suggest that hyperhomocysteinemia plays a major role in the development of cerebral small vessel ischemia, but not in the development of atherosclerosis of major cerebral arteries.

Different risk factor profiles between silent brain infarction and symptomatic lacunar infarction.

BACKGROUND/AIMS: It is generally assumed that silent brain infarction (SBI) and symptomatic lacunar infarction (sLAC) share common vascular risk factors and their pathogeneses are known to be similar. However, few studies have conducted a risk factor profile analysis of the two diseases in a single study design. METHODS: This study included 64 subjects with SBI lesions, 140 patients with sLAC, and 342 controls by retrospective investigation of brain MRI. Topographic findings and vascular risk factor profiles were compared. RESULTS AND CONCLUSION: Compared to the controls, the SBI group was found to be associated with hypertension (p = 0.002) and elevated plasma total homocysteine level (p = 0.02). The sLAC group was found to be associated with hypertension (p = 0.001), diabetes (p = 0.004), smoking (p = 0.002), ischemic heart disease (p = 0.01) and hyperlipidemia (p = 0.04). In the present study, risk factor profiles of the SBI and sLAC were not exactly the same, indicating a different pathogenesis between the two diseases.