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Abstract Background Intracranial atherosclerotic disease (ICAD) represents a leading cause of ischemic stroke worldwide, conferring increased risk of recurrent stroke and poor clinical outcomes among stroke survivors. Emerging evidence indicates a paradigm shift, pointing towards increasing detection rates of ICAD among White populations and an evolving epidemiological profile across racial and ethnic groups. The present review aims to provide a comprehensive overview of ICAD, focusing on its pathophysiology, diagnostic approach, and evolving epidemiological trends, including underlying mechanisms, advanced neuroimaging techniques for diagnostic evaluation, racial disparities in prevalence, and current and emerging management strategies. Main body Atherosclerotic plaque accumulation and progressive arterial stenosis of major intracranial arteries comprise the pathophysiological hallmark of ICAD. In clinical practice, the diagnosis of intracranial artery stenosis (ICAS) or high-grade ICAS is reached when luminal narrowing exceeds 50% and 70%, respectively. Advanced neuroimaging, including high-resolution vessel wall MRI (HRVW-MRI), has recently enabled ICAD detection before luminal stenosis occurs. While earlier studies disclosed significant racial disparities in ICAS prevalence, with higher rates among Asians, Hispanics, and Blacks, recent evidence reveals rising detection rates of ICAD among White populations. Genetic, environmental and epigenetic factors have been suggested to confer an increased susceptibility of certain ethnicities and races to ICAD. Nevertheless, with improved accessibility to advanced neuroimaging, ICAD is increasingly recognized as an underlying stroke etiology among White patients presenting with acute ischemic stroke and stroke of undetermined etiology. While conventional management of ICAS entails risk factor modification, pharmacotherapy, and endovascular treatment in selected high-risk patients, substantial progress remains to be made in the management of ICAD at its early, pre-stenotic stages. Conclusion ICAD remains a critical yet underappreciated risk factor for ischemic stroke across all populations, highlighting the need for increased awareness and improved diagnostic strategies. The emerging epidemiological profile of ICAD across racial groups necessitates a reassessment of risk factors, screening protocols and preventive strategies. Future research should focus on refining the diagnostic criteria and expanding the therapeutic options to cover the full spectrum of ICAD, with the aim of improving patient outcomes and reducing the global burden of intracranial atherosclerosis and stroke.

Research investigating pragmatic deficits in individuals with right hemisphere damage focuses on identifying the potential mechanisms responsible for the nature of these impairments. Nonetheless, the presumed shared cognitive mechanisms that could account for these deficits have not yet been established through data-based evidence from lesion studies. This study aimed to examine the co-occurrence of pragmatic language deficits, Theory of Mind impairments, and executive functions while also exploring their associations with brain lesion sites. Twenty-five patients suffering from unilateral right hemisphere stroke and thirty-seven healthy participants were recruited for this study. The two groups were tested in pragmatics, Theory of Mind, and executive function tasks. Structural imaging data were also obtained for the identification of the lesion sites. The findings of this study suggest a potential convergence among the three aforementioned cognitive mechanisms. Moreover, we postulate a hypothesis for a neural circuitry for communication impairments observed in individuals with right hemisphere damage.

Neurobrucellosis presents in various clinical forms and should always be considered in neurological patients in highly endemic areas such as the Mediterranean basin. Establishing a diagnosis can be challenging since serological testing can sometimes yield negative results. We present a rare case of a seronegative relapse of neurobrucellosis in a patient who had been successfully treated for systemic brucellosis. Oligoclonal bands, an agglutination test, and 16S rRNA sequencing of cerebrospinal fluid proved essential in unmasking a confined central nervous system relapse. This case reinforces the need for establishing diagnostic criteria for neurobrucellosis, which could potentially include oligoclonal bands and an agglutination test on the cerebrospinal fluid.

Objectives: Nondipping pattern of nocturnal blood pressure is associated with silent ischemic cerebrovascular lesions and lacunar infarctions. In this case-control study, we aimed to evaluate the association of diurnal blood pressure variation with the occurrence of intracerebral hemorrhage., Methods: Ambulatory blood pressure monitoring was performed at 21-28 days after ictus in 78 first-ever unselective consecutive patients with intracerebral hemorrhage and in 80 age-adjusted and sex-adjusted controls who were referred to the hypertension center of our institution. The degree of nocturnal blood pressure dip was calculated as [(mean daytime values-mean night-time values)/mean daytime values]x100. Nondippers were defined as patients who exhibited a <10% nocturnal dip in systolic blood pressure. Logistic regression models were constructed to assess the association of nondipping status with intracerebral hemorrhage after adjusting for potential confounders (cardiovascular risk factors, office and ambulatory blood pressure levels)., Results: Prevalence of nondipping was significantly greater among cases than among controls (74.4% vs. 43.8%, P<0.001). Nondipping status was independently (P=0.033) associated with intracerebral hemorrhage (OR: 2.326, 95% CI: 1.068-5.050) in a multiple variable logistic regression model that adjusted for baseline characteristics, cardiovascular risk factors, office and ambulatory blood pressure variables. The magnitude of the nocturnal systolic blood pressure dipping was inversely related to the risk of intracerebral bleeding; the odds ratio for intracerebral hemorrhage associated with every 1% decrease in nocturnal systolic blood pressure dip was 1.143 (95% CI: 1.058-1.235, P=0.001)., Conclusions: Given the previous reports that nondipping contributes to the risk of cerebral infarction, our results indicate that blunted nocturnal blood pressure dip may be also associated with the occurrence of intracerebral hemorrhage.