In spite of high prevalence and clinical relevance of leukoaraiosis (LA), its pathophysiology is still incompletely understood. Theories of ischaemic genesis and a leaky blood–brain barrier are contradictory yet could share a common denominator–endothelial dysfunction (cerebral, systemic or both), which has not been studied thoroughly in LA. Thirty patients with LA (58 years (SD 7)) and 30 gender- and age-matched controls without LA (55 years (SD 6)) were recruited. The vascular risk factors (VRF) were identical in both groups. Cerebral endothelial function was determined by cerebrovascular reactivity to L-arginine (CVR). Systemic endothelial function was determined by flow-mediated dilatation (FMD) of the brachial artery after hyperaemia. All participants underwent a brain MRI to search for radiological signs of LA that was classified according to the Fazekas score. Linear regression was used to explore the correlation between CVR and FMD in patients with LA. A 95 % confidence interval was used. For any statistical test used in the study, p ≤ 0.050 was regarded as statistically significant. We found a marked and significant decrease in both CVR (9.6 % (SD 3.2) vs. 15.8 % (SD 6.1), p < 0.001) and FMD (4.8 % (SD 3.1) vs. 7.4 % (SD 3.8), p = 0.004) in LA patients compared to controls. Both CVR (7.4 % (SD 3.1) vs. 12.2 % (SD 2.6), p = 0.001) and FMD (3.0 % (SD 2.2) vs. 6.4 % (SD 3.1), p = 0.011) were significantly decreased in LA subgroup Fazekas 3 compared to subgroup Fazekas 1. CVR and FMD significantly positively correlated (b = 0.192, 95 % CI = 0.031–0.354, p = 0.02). The results of our pilot study suggest that patients with LA have a significant impairment of both cerebral and systemic endothelial function that is larger than could be expected based on present VRF. Endothelial dysfunction increases in parallel with LA severity and correlates between cerebral and systemic arterial territory. Overall, our results suggest a so far unknown “intrinsic” generalised endothelial dysfunction in patients with LA that could be involved in LA pathophysiology. This interesting issue needs to be confirmed in larger samples since it could help better understand the mechanisms underlying LA.

Pathogenesis of Leukoaraiosis: A Review | InTechOpen, Published on: 2016-10-26. Authors: Matija Zupan

Cerebral hyperperfusion syndrome (CHS) is a serious post-procedural complication of carotid artery stenting (CAS). The pathophysiological mechanisms of CHS in the absence of arterial hypertension (AH) remain only partially understood. We performed a systematic literature search of the PubMed database using the terms »cerebral hyperperfusion syndrome«, »hypotension«, »hyperperfusion«, »stroke«, »intracranial hemorrhages«, »risk factors«, »carotid revascularization«, »carotid stenting«, »carotid endarterectomy«, »blood-brain barrier«, »endothelium«, »contrast encephalopathy«, and combinations. We present a case of a normotensive female patient who developed CHS post-CAS for symptomatic carotid stenosis while being hypotensive with complete recovery. We identified 393 papers, among which 65 were deemed relevant to the topic. The weighted average prevalence of CHS after CAS is 1.2% [0.0–37.7%] with that of intracranial hemorrhage (ICH) being 0.51% [0–9.3%]. Recently symptomatic carotid stenosis or contralateral carotid revascularization, urgent intervention, acute carotid occlusion, contralateral ≥70% stenosis, and the presence of leptomeningeal collaterals were associated with CHS. A prolonged hemodynamic instability after CAS conveys a higher risk for CHS. However, none of the articles mentioned isolated hypotension as a risk factor for CHS. Whereas mortality after ICH post-CAS ranges from 40 to 75%, in the absence of ICH, CHS generally carries a good prognosis. AH is not obligatory in CHS development. Even though impaired cerebral autoregulation and post-revascularization changes in cerebral hemodynamics seem to play a pivotal role in CHS pathophysiology, our case highlights the complexity of CHS, involving factors like endothelial dysfunction and sudden reperfusion. Further research is needed to refine diagnostic and management approaches for this condition.

Background: Stroke expertise is critical for timely and appropriate intravenous thrombolysis (IVT) and affects IVT use. Introduction: In Slovenia, IVT is administered in general hospitals, which often lack on-site neurologic expertise. To overcome this obstacle, a national telestroke network, TeleKap, has been implemented. The aim of the study was to determine whether TeleKap is associated with enhanced IVT use. Materials and Methods: This investigation was a retrospective observational study comparing the number of acute ischemic stroke (AIS) patients and the use of IVT during the first 3 consecutive years. TeleKap, a decentralized hub-and-spoke telestroke model covering the entire nation, consists of one comprehensive stroke center and 12 spokes classified according to the availability of on-site neurologic expertise. Results: During the observation period, we treated a total of 1,316 patients with AIS, of which 508 (38.6%) received IVT. We found statistically significant positive trends in the number of IVT patients (142 in 2015, 158 in 2016, and 208 in 2017; B = 4.39, standard error (SE) = 1.59, p  = 0.01) and the number of AIS patients (326 in 2015, 424 in 2016, and 566 in 2017; B = 14.42, SE = 5.19, p  = 0.01) for all spokes. The trend in the IVT rate was numerically negative but did not reach statistical significance (43.5% in 2015, 37.3% in 2016, and 36.7% in 2017; p  = 0.30). Discussion: TeleKap enhanced IVT use regardless of on-site neurologic expertise. Conclusions: TeleKap proved to be efficient. It could serve as a model of telestroke care for other similar countries.