Purpose The purpose of this study was to investigate the effect of dexmedetomidine (DEX) on hypotension-induced neuronal damage in a chronic cerebral hypoperfusion (CCH) model of rats, an established model of cerebral white matter lesions (WML) in humans, which is prevalent in the elderly and closely related to cognitive decline. Methods The CCH model rats were randomly assigned to one of four groups: normotension + no DEX (NN) group (n = 6), normotension + DEX (ND) group (n = 6), hypotension + no DEX (HN) group (n = 6), or hypotension + DEX (HD) group (n = 6). Under isoflurane anesthesia, mean arterial blood pressure was maintained at or above 80 mmHg (normotension) or below 60 mmHg (hypotension) for a duration of two hours. The DEX groups received 50 μg of DEX intraperitoneally. Two weeks later, the Y-maze test and, after preparing brain slices, immunohistochemical staining were performed using antibodies against neuronal nuclei (NeuN), microtubule-associated protein 2 (MAP2), glial fibrillary acidic protein (GFAP), and Ionized calcium-binding adapter molecule 1 (Iba1). Results Behavioral observations showed no significant differences among the groups. Significant reductions of both NeuN-positive cells and the MAP2-positive area were found in the hippocampal CA1 in the HN group compared with NN and ND groups, but not in the HD group. GFAP and Iba-1-positive areas were significantly increased in the HN group, but not in the HD group. Conclusion DEX significantly ameliorated hypotension-induced neuronal damage and both astroglial and microglial activation in the CA1 region of CCH rats.

White matter lesion (WML), also known as white matter hyperintensities or leukoaraiosis, was first termed in 1986 to describe the hyperintense signals on T2-weighted imaging (T2WI) and fluid-attenuated inversion recovery (FLAIR) maps. Over the past decades, a growing body of pathophysiological findings regarding WMLs have been discovered and discussed. Currently, the generally accepted WML pathogeneses mainly include hypoxia-ischemia, endothelial dysfunction, blood-brain barrier disruption, and infiltration of inflammatory mediators or cytokines. However, none of them can explain the whole dynamics of WML formation. Herein, we primarily focus on the pathogeneses and neuroimaging features of vascular WMLs. To achieve this goal, we searched papers with any type published in PubMed from 1950 to 2020 and cross-referenced the keywords including \"leukoencephalopathy\", \"leukoaraiosis\", \"white matter hyperintensity\", \"white matter lesion\", \"pathogenesis\", \"pathology\", \"pathophysiology\", and \"neuroimaging\". Moreover, references of the selected articles were browsed and searched for additional pertinent articles. We believe this work will supply the robust references for clinicians to further understand the different WML patterns of varying vascular etiologies and thus make customized treatment.

Prediction of intracerebral hematoma expansion (IHE) is of critical importance during intracerebral hemorrhage (ICH) management. Given its suggested positive connection with cerebral microvascular disease status, intracranial internal carotid artery wall calcifications (ICAC) on admission computed tomography (CT) studies may contribute to prediction of IHE.
Presence, burden and type [as per Kockelkoren\'s score] of ICAC were defined in admission CT and CT-angiography of 201 ICH patients [mean age: 70 ± 13 years, 44 % female]. A Kockelkoren\'s score of <7 indicated intimal calcification [iICAC], while ≥7 indicated non-intimal [or medial] ones [mICAC]. IHE criteria were absolute volume increase of ≥12.5cc or ≥6cc, and relative increase ≥33 % or ≥26 %.
ICAC was diagnosed in 79.6 % of ICH patients. ICAC status was not independent indicator of milder IHE (≥6cc and ≥26 % IHE, both in 27 %). Presence of contralateral mICAC was found to be an independent predictor for higher grade IHE (expβ = 3.44, 95 %CI: 1.47-8.04, for IHE ≥ 12.5cc, diagnosed in 14.4 %; and expβ = 2.67, 95 %CI: 1.29-5.55, for IHE ≥ 33 %, diagnosed in 24 %). Mortality (31 %) was higher in those with ipsilateral any type ICAC (36 % in mICAC, 38 % in iICAC, 17 % in no ICAC, p = 0.017), but this was not independent predictor in logistic regression. Similarly, medial ICAC in both ipsilateral (47 % vs. 31 %, p = 0.037) and contralateral (47 % vs. 30 %, p = 0.017) sides was associated with poorer prognosis (42 %) on univariate, but not multivariate analysis.
Intracranial ICA calcification is highly prevalent in ICH. mICAC may be associated with risk of \"high amount\" acute hematoma expansion, hospital mortality and poor prognosis.

OBJECTIVE: Neurological symptom severity is a prognostic factor for post-stroke activities of daily living (ADL). Recently, it has been reported that white matter lesions indicate poor functional prognosis in patients with stroke. The present study investigated the influence of white matter lesions on the ADL of older patients with stroke who have mild neurological symptoms.
METHODS: We investigated ADL at discharge in 44 patients with stroke (men, n = 27; women, n = 17; mean age 78 years [range 71-85 years]) aged ≥65 years with National Institutes of Health Stroke Scale scores of ≤5 (cerebral infarction, n = 37; cerebral hemorrhage, n = 7). We used single correlation analysis and multiple regression analysis to investigate factors that correlated with ADL at discharge. ADL at discharge was also evaluated on the basis of white matter lesion severity (Fazekas classification, grades 0-3).
RESULTS: Single correlation analysis showed that age (r = -0.36, P = 0.016), male sex (r = 0.362, P = 0.016), neurological symptom severity (r = -0.361, P = 0.016), ADL on starting rehabilitation (r = 0.685, P < 0.001) and white matter lesion severity (r = -0.361, P = 0.016) significantly correlated with ADL at discharge. Multiple regression analysis showed that ADL on starting rehabilitation (β = 0.519, t = 4.723, P < 0.001) and white matter lesion severity (β = -0.309, t = -3.057, P < 0.01) were statistically significant prognostic factors for ADL at discharge. ADL at discharge score was significantly lower in the group with high white matter lesion severity (Fazekas, grade 2) than in the other two groups (Fazekas, grade 0, P < 0.01; Fazekas, grade 1, P < 0.05).
CONCLUSIONS: Severe white matter lesions are a prognostic factor for poor ADL at discharge in older patients with stroke who have mild neurological symptoms. Geriatr Gerontol Int 2016; 16: 942-947.