The perception of music can be impaired after a stroke. This dysfunction is called amusia and amusia patients often also show deficits in visual abilities, language, memory, learning, and attention. The current study investigated whether deficits in music perception are selective for musical input or generalize to other perceptual abilities. Additionally, we tested the hypothesis that deficits in working memory or attention account for impairments in music perception. Twenty stroke patients with small infarctions in the supply area of the middle cerebral artery were investigated with tests for music and visual perception, categorization, neglect, working memory and attention. Two amusia patients with selective deficits in music perception and pronounced lesions were identified. Working memory and attention deficits were highly correlated across the patient group but no correlation with musical abilities was obtained. Lesion analysis revealed that lesions in small areas of the putamen and globus pallidus were connected to a rhythm perception deficit. We conclude that neither a general perceptual deficit nor a minor domain general deficit can account for impairments in the music perception task. But we find support for the modular organization of the music perception network with brain areas specialized for musical functions as musical deficits were not correlated to any other impairment.

We evaluated the clinical outcomes of malignant middle cerebral artery (MCA) infarction (MMI) and determined an infarcted brain volume (BV) threshold value for accurate MMI prediction in elderly patients.

Malignant middle cerebral artery infarction (mMCAi) is a serious complication of cerebral infarction usually associated with poor patient prognosis. In this retrospective study, we analyzed clinical information as well as non-contrast computed tomography (NCCT) and computed tomography angiography (CTA) data from patients with cerebral infarction in the middle cerebral artery (MCA) territory acquired within 24 h from symptoms onset. Then, we aimed to develop a model based on the radiomics signature to predict the development of mMCAi in cerebral infarction patients. Patients were divided randomly into training (n = 87) and validation (n = 39) sets. A total of 396 texture features were extracted from each NCCT image from the 126 patients. The least absolute shrinkage and selection operator regression analysis was used to reduce the feature dimension and construct an accurate radiomics signature based on the remaining texture features. Subsequently, we developed a model based on the radiomics signature and Alberta Stroke Program Early CT Score (ASPECTS) based on NCCT to predict mMCAi. Our prediction model showed a good predictive performance with an AUC of 0.917 [95% confidence interval (CI), 0.863-0.972] and 0.913 [95% CI, 0.795-1] in the training and validation sets, respectively. Additionally, the decision curve analysis (DCA) validated the clinical efficacy of the combined risk factors of radiomics signature and ASPECTS based on NCCT in the prediction of mMCAi development in patients with acute stroke across a wide range of threshold probabilities. Our research indicates that radiomics signature can be an instrumental tool to predict the risk of mMCAi.

We aimed to explore potential cytokines involved in the malignant middle cerebral artery infarction (MMI) and elucidate their underlying regulatory mechanisms.

Based on randomized controlled trials (RCTs), clinical guidelines for the treatment of space-occupying hemispheric infarct employ age (≤60 yr) and time elapsed since stroke onset (≤48 h) as decisive criteria whether to perform decompressive craniectomy (DC). However, only few patients in these RCTs underwent DC after 48 h.

Malignant middle cerebral artery infarction (mMCA) is a devastating disease with rates of fatality as high as 80%. Decompressive hemicraniectomy (DHC) reduces mortality, but many survivors inevitably remain severely disabled. This study aimed to analyze patients with mMCA undergoing DHC or best medical treatment (BMT) baseline characteristics and factors linked to therapeutic choice and determinants of prognosis.

Interspecies variability and poor clinical translation from rodent studies indicate that large gyrencephalic animal stroke models are urgently needed. We present a proof-of-principle study describing an alternative animal model of malignant infarction of the middle cerebral artery (MCA) in the common pig and illustrate some of its potential applications. We report on metabolic patterns, ionic profile, brain partial pressure of oxygen (PtiO2), expression of sulfonylurea receptor 1 (SUR1), and the transient receptor potential melastatin 4 (TRPM4).

Strokectomy means surgical excision of infarcted brain tissue post-stroke with preservation of skull integrity, distinguishing it from decompressive hemicraniectomy. Both can mitigate malignant middle cerebral artery (MCA) syndrome but evidence regarding strokectomy is sparse. Here, we report our data and meta-analysis of strokectomy compared to hemicraniectomy for malignant MCA infarction. All malignant MCA stroke cases requiring surgical intervention in a large tertiary centre (January 2012-December 2017, N = 24) were analysed for craniotomy diameter, complications, length of follow-up and outcome measured using the modified Rankin score (mRS). Good outcome was defined as mRS 0-3 at 12 months. In a meta-analysis, outcome from strokectomy (pooled from our cohort and published strokectomy studies) was compared with hemicraniectomy (our cohort pooled with published DECIMAL, DESTINY and HAMLET clinical trial data). In our series (N = 24, 12/12 F/M; mean age: 45.83 ± 8.91, range 29-63 years), 4 patients underwent strokectomy (SC) and 20 hemicraniectomy (HC). Among SC patients, craniotomy diameter was smaller, relative to HC patients (86 ± 13.10 mm, 120 ± 4.10 mm, respectively; p = 0.003), complications were less common (25%, 55%) and poor outcomes were less common (25%, 70%). In the pooled data (N = 41 SC, 71 HC), strokectomy tended towards good outcome more than hemicraniectomy (OR 2.2, 95% CI 0.99-4.7; p = 0.051). In conclusion, strokectomy may be non-inferior, lower risk and cost saving relative to hemicraniectomy sufficiently to be worthy of further investigation and maybe a randomised trial.

Puerarin, a major isoflavonoid derived from the Chinese medical herb Radix puerariae (kudzu root), has been reported to be useful in the treatment of various cardiovascular diseases. In the present study, we examined the detailed mechanisms underlying the inhibitory effects of puerarin on inflammatory and apoptotic responses induced by middle cerebral artery occlusion (MCAO) in rats. Treatment of puerarin (25 and 50 mg/kg; intraperitoneally) 10 min before MCAO dose-dependently attenuated focal cerebral ischemia in rats. Administration of puerarin at 50 mg/kg, showed marked reduction in infarct size compared with that of control rats. MCAO-induced focal cerebral ischemia was associated with increases in hypoxia-inducible factor-1alpha (HIF-1alpha), inducible nitric oxide synthase (iNOS), and active caspase-3 protein expressions as well as the mRNA expression of tumor necrosis factor-alpha (TNF-alpha) in ischemic regions. These expressions were markedly inhibited by the treatment of puerarin (50 mg/kg). In addition, puerarin (10-50 microM) concentration-dependently inhibited respiratory bursts in human neutrophils stimulated by formyl-Met-Leu-Phe. On the other hand, puerarin (20-500 microM) did not significantly inhibit the thiobarbituric acid-reactive substance reaction in rat brain homogenates. An electron spin resonance (ESR) method was conducted on the scavenging activity of puerarin on the free radicals formed. Puerarin (200 and 500 microM) did not reduce the ESR signal intensity of hydroxyl radical formation. In conclusion, we demonstrate that puerarin is a potent neuroprotective agent on MCAO-induced focal cerebral ischemia in vivo. This effect may be mediated, at least in part, by the inhibition of both HIF-1alpha and TNF-alpha activation, followed by the inhibition of inflammatory responses (i.e., iNOS expression), apoptosis formation (active caspase-3), and neutrophil activation, resulting in a reduction in the infarct volume in ischemia-reperfusion brain injury. Thus, puerarin treatment may represent a novel approach to lowering the risk of or improving function in ischemia-reperfusion brain injury-related disorders.

Background: Cerebral venous drainage might influence brain edema characteristics and functional outcome of patients with severe ischemic stroke. The purpose of the study was to evaluate whether hypoplasia of transverse sinuses or the internal jugular veins is associated with poor functional outcome in patients with space-occupying middle cerebral artery (MCA) infarction who underwent decompressive surgery. Methods: We performed a retrospective analysis of patients with space-occupying MCA infarction treated with decompressive surgery at our university hospital. The transverse sinuses and the internal jugular veins were evaluated on baseline images and categorized as normal, hypoplastic or occluded. We defined composite variables for ipsilateral, contralateral or any abnormal cerebral venous drainage. We assessed the functional outcome at 12 months with the modified Rankin scale (mRS) score and defined poor functional outcome as mRS scores 5 and 6. Results: We analyzed 88 patients with available baseline imaging data [mean [SD] patient age 53 (±9) years; median[IQR] time to decompressive surgery 31(22-51) h]. At 12 months 44 patients (50%) had a poor outcome. In univariate analysis neither ipsilateral (OR 1.98;95%CI: 0.75-5.40), nor contralateral (OR 1.56;95%CI: 0.59-4.24) or any (OR 1.6; 95%CI: 0.68-3.79) hypoplasia or occlusion of venous drainage were significantly associated with poor functional outcome. In multivariate analyses, higher patient age (OR 1.07;95%CI 1.01-1.14) and baseline stroke severity (OR 3.42;95%CI 1.31-9.40) were independent predictors of poor functional outcome, but not ipsilateral hypoplasia or occlusion of venous drainage (OR 1.31;95%CI 0.47-3.67). Conclusions: The cerebral venous drainage pattern was not significantly associated with poor functional outcome in our cohort of patients with space-occupying MCA infarction who underwent decompressive surgery.

Intracranial atherosclerotic stroke occurs through various mechanisms, mainly by artery-to-artery embolism (AA) or branch occlusive disease (BOD). This study evaluated the spatial relationship between middle cerebral artery (MCA) plaques and perforating arteries among different MCA territory infarction types using vessel wall magnetic resonance imaging (VW-MRI).

Early progressive infarction (EPI) is frequently observed and related to poor functional outcome in patients with middle cerebral artery (MCA) infarction caused by MCA occlusion. We evaluated the perfusion parameters of magnetic resonance imaging (MRI) as a predictor of EPI.

Moderate hypothermia after decompressive surgery might not be beneficial for stroke patients. However, normothermia may prove to be an effective method of enhancing neurological outcomes. The study aims were to evaluate the application of a pre-specified normothermia protocol in stroke patients after decompressive surgery and its impact on temperature load, and to describe the functional outcome of patients at 12 months after treatment.

Decompressive hemicraniectomy decreases mortality and severe disability from space-occupying middle cerebral artery infarction in selected patients. However, attitudes towards hemicraniectomy for dominant-hemispheric stroke have been hesitant. This systematic review and meta-analysis examines the association of stroke laterality with outcome after hemicraniectomy.

To evaluate the utility of high-resolution vessel wall imaging (HR-VWI) of middle cerebral artery (MCA), and to compare HR-VWI findings between striatocapsular infarction (SC-I) and lenticulostriate infarction (LS-I).

This study examines if involvement of the lenticulostriate arteries (LSAs) in MCA stroke and consecutive infarction of the basal ganglia can be predicted by the exact occlusion site, as determined in pre-interventional CT or MRI imaging.

In ischemic stroke, vasopressin hypersecretion is a critical factor of cerebral swelling and brain injury. To clarify neural mechanisms underlying ischemic stroke-evoked vasopressin hypersecretion, we observed the effect of unilateral permanent middle cerebral artery occlusion (MCAO) in rats on astrocytic plasticity and vasopressin neuronal activity in the supraoptic nucleus (SON) as well as their associated cerebral injuries. MCAO for 8 hr caused cerebral infarction in the MCAO side where water contents also increased. Immunohistochemical examination revealed that the percentage of phosphorylated extracellular signal-regulated protein kinase 1/2 (pERK1/2)-positive vasopressin neurons in the SON of MCAO side was significantly higher than that in non-MCAO side and in sham group. In the cortex, pERK1/2 and aquaporin 4 expressions increased significantly in the infarction area, while glial fibrillary acidic protein (GFAP) reduced significantly compared with the noninfarction side in brain cortex. Microinjection of N-(1,3,4-Thiadiazolyl)nicotinamide-020 [TGN-020, a specific blocker of aquaporin 4] into the SON blocked MCAO-evoked increases in pERK1/2 in the SON as well as the reduction of GFAP and the increase in pERK1/2 and aquaporin 4 in the infarction area of the cortex. Finally, oxygen and glucose deprivation reduced GFAP expression and the colocalization and molecular association of GFAP with aquaporin 4 in the SON in brain slices. These effects were blocked by TGN-020 and/or phloretin, a blocker of astrocytic volume-regulated anion channels. These findings indicate that blocking aquaporin 4 in the SON may reduce the activation of vasopressin neurons and brain injuries elicited by vasopressin during ischemic stroke.

To estimate evidence for decompressive hemicraniectomy (DHC) versus medical treatment effects on survival rate and favorable functional recovery among patients of malignant middle cerebral artery infarction (MMCAI) in randomized controlled trials (RCTs).

The aim of this study was to research the mechanism of proprotein convertase subtilisin-like kexin type 9 (PCSK9) inhibitor in neural protective effect on rat cerebral ischemic reperfusion injury (I/RI). The transient middle cerebral artery occlusion (tMCAO) model of rats was prepared by the suture method, and PCSK9 inhibitor was injected intraperitoneally immediately after I/R. The rats were scored for neurological deficits and the cerebral infarction volume was measured. The brain tissues were collected and western blot (WB) was used to detect the expression of PCSK9. The rat cortical neural stem cells were treated with oxygen glucose deprivation (OGD) to establish a cell model of ischemia/reperfusion. WB was used to detect the expression of PCSK9 and the apoptosis-related pathway proteins. After interfering with the expression of PCSK9 siRNA, the cell viability (cell counting kit-8 assay) and apoptosis (TUNEL staining, Annexin V/PI method) were detected, and the cell proliferation was detected by EdU staining and flow cytometry. The expression of PCSK9 in the brain tissue of the MCAO group was dramatically increased. PCSK9 inhibitor can improve neurobehavioral scores and reduce apoptosis and infarct volume. An OGD model of neural stem cells in vitro was constructed. Inhibiting PCSK9 with si-PCSK9 can increase cell viability, promote cell proliferation, and also reduce cell apoptosis. Inhibition of PCSK9 can decrease the cerebral infarct volume in rats with cerebral I/RI and improve the neural function. Mechanically, inhibition of PCSK9 can lead to the decrease of nerve cell apoptosis and promotion of cell proliferation.

Pathological yawning is a compulsive, frequent, repetitive yawning triggered by a specific reason besides fatigue or boredom. It may be related to iatrogenic, neurologic, psychiatric, gastrointestinal, or metabolic disorders. Moreover, it could also be seen in the course of an ischemic stroke.