Thrombus age does not differentiate between cardiogenic and atherosclerotic strokes

Objective Interventional stroke therapy made thrombi available for histological analysis. Unfortunately, simple composition aspects such as erythrocyte versus fibrin/platelet rich did not allow a feasible allocation to thrombi’s cardiac or carotid origin. Since the mentioned criteria represent characteristics of thrombus age, we used established histological criteria for determining thrombus age in patients who had an atherosclerotic (TOAST (Trial of Org 10172 in Acute stroke Treatment) 1) stroke versus patients who had a cardioembolic (TOAST 2) stroke.Methods We assessed prospectively data from stroke patients presenting with occlusion of the middle cerebral artery eligible for catheter-based intervention. Besides patient characteristics and stroke workup, extracted thrombi were classified into different age categories according to their cellular to fibrotic transition. Thrombi were collected in an erythrocyte lysing solution to reduce acute clotting effects. Statistics were done with a non-parametric Kolmogorov-Smirnov test.Results 170 patients were included, of which 50 (38 men; 73±12 years) had a TOAST 1 and 99 (59 women; 75±10 years) had a TOAST 2 categorised stroke. Age, National Institutes of Health Stroke Score (13±7 vs 15±7), Alberta Stroke Program Early CT Score (9±3 vs 9±2), Thrombolysis in Cerebral Infarction Score (2.9±0.2 vs 2.9±0.3), modified Rankin Score on discharge (3.2±2 vs 3.2±2), number of vascular risk factors (0.9±1.4 vs 1.0±1.1) or time span between symptom onset to reperfusion (266±115 vs 260±128 min) remained non-significant. Also, thrombus age did not differ between the groups. The mean age of thrombi was 5–8 days. However, the male–female ratio differed significantly (p<0.0005) between groups, with more men in TOAST 1 group and more women in TOAST 2 group.Conclusion Age aspects of thrombi seem not feasible to allow reliable source allocation. However, the young age of thrombi points to a rapid detachment. The difference in sex relation is in line with previous reports

Effects of anti-inflammatory vagus nerve stimulation on the cerebral microcirculation in endotoxinemic rats

Abstract Background In sepsis syndromes the severity of the inflammation triggers microvascular dysfunction and early organ failure. We studied the effects of anti-inflammatory vagus nerve stimulation on the cerebral microcirculatory integrity in an endotoxinemic rat model. Methods In both control and endotoxinemic (5 mg/kg lipopolysaccharide i.v.) rats, the effect of cervical bilateral vagotomy with or without left-sided distal vagus nerve stimulation were compared to non-vagotomized, nonstimulated group (sham). Neurovascular coupling was analyzed by electrical forepaw stimulation, EEG, and cortical laser-Doppler flow recording. Resting cerebral blood flow, evoked potentials and hemodynamic responses, were obtained over a period of 4.5 hours. Regulation of the nitric oxide system (iNOS expression and nitrite/nitrate measurements), cytokines (IFN-γ, TNF-α, IL-6, IL-10), hypoxic and apoptosis signaling molecules (HIF-2α, Bax) were measured at the end of experiments. Results In endotoxinemic rats, vagus nerve stimulation tended to increase anti-inflammatory cytokine levels and resulted in a stabile hemodynamic response (28 ± 13%; versus baseline). Vagotomized animals incurred a pro-inflammatory response (7 ± 4%; P P  Conclusions Vagus nerve stimulation in endotoxinemic rats had a positive effect on neurovascular coupling and stabilized evoked potentials.</p

Visually evoked cerebral vasomotor response in smoking and nonsmoking young adults, investigated by functional transcranial Doppler

Smoking has been known to cause endothelial dysfunction and is an important risk factor for ischemic stroke. In our study we investigated whether chronic cigarette smoking affects the cerebral blood flow velocity response to a physiological, visual stimulus. By using a visual cortex stimulation paradigm, the flow velocity response in the posterior cerebral arteries (PCA) was measured bilaterally, in 32 young healthy adults (16 smokers, 16 nonsmokers). The stimulation protocol consisted of 10 cycles with a resting phase of 20 s and a stimulating phase of 40 s for each cycle. Besides functional transcranial Doppler (TCD), laboratory tests and measurement of intima-media-thickness (IMT) were also performed. Repeated-measure analysis of variance (ANOVA) was used to detect differences in visually evoked relative flow velocity time courses between smokers and nonsmokers. Repeated-measure ANOVA revealed marked difference in the peak systolic flow velocity time courses between smokers and nonsmokers (p< .001). Maximum percent change of visually evoked flow velocity after visual stimulation was 19+/-4% and 30+/-3% in smokers and nonsmokers, respectively (p< .0001). IMT values did not indicate atherosclerosis in young smokers. Infectious disease and hyperlipidemia were also ruled out by measurement of sensitive C-reactive protein and serum lipids. This is the first functional TCD study demonstrating impaired visually evoked flow velocity response caused by chronic cigarette smoking in otherwise healthy, young subjects. The impaired cerebral vasodilatory mechanism together with atherosclerosis may influence stroke occurrence and outcome in chronic smokers

Hypocapnia induced vasoconstriction significantly inhibits the neurovascular coupling in humans

Background/aims: Previous studies proved that vasodilation, caused by hypercapnia or acetazolamide, does not inhibit the visually evoked flow velocity changes in the posterior cerebral arteries. Our aim was to determine whether vasoconstriction induced by hypocapnia affects the neurovascular coupling. Methods: By using a visual cortex stimulation paradigm, visually evoked flow velocity changes were detected by transcranial Doppler sonography in both posterior cerebral arteries of fourteen young healthy adults. The control measurement was followed by the examination under hyperventilation. Visual-evoked-potentials were also recorded during the control and hyperventilation phases. Results: The breathing frequency increased from 16 +/- 2 to 37 +/- 3/min during hyperventilation, resulting in a decrease of the end-tidal CO(2) from 37 +/- 3 to 25 +/- 3 mm Hg and decrease of resting peak systolic flow velocity from 58 +/- 11 to 48 +/- 11 cm/s (p<0.01). To allow comparisons between volunteers, relative flow velocity was calculated in relation to baseline. Repeated measures analysis of variance revealed significant difference between the relative flow velocity time courses during hyper- and normoventilation (p<0.001). The maximum changes of visually evoked relative flow velocities were 26 +/- 7% and 12 +/- 5% during normoventilation and hyperventilation, respectively (p<0.01). Visual-evoked-potentials did not differ in the control and hyperventilation phases. Conclusion: The significantly lower visually evoked flow velocity changes but preserved visual-evoked-potential during hyperventilation indicates that the hypocapnia induced vasoconstriction significantly inhibits the neuronal activity evoked flow response. (C) 2011 Elsevier B.V. All rights reserved