Correlation of silent brain infarcts and leukoaraiosis in middle-aged ischemic stroke patients: a retrospective study

So your competent? doctor is required to have EXACT PROTOCOLS that restore myelin. Is your doctor competent in this regard? Or don't you have a functioning stroke doctor? Does your doctor even know this problem needs to be fixed?

 Leukoaraiosis is the rarefaction of the brain white matter caused by loss of axons and myelin due to ischemic injury and appears to be of central importance in the neurocognitive defects associated with HD.

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Correlation of silent brain infarcts and leukoaraiosis in middle-aged ischemic stroke patients: a retrospective study

Mohammad Fathi Abdulsalam¹Nour Shaheen^2*†Ahmed Shaheen²Yasmeen Jamal Alabdallat³Abdelraouf Ramadan⁴Mostafa Meshref¹Fathy Mahmoud Mansour¹Elsayed Abed¹Abdel-Ghaffar I. Fayed¹Mohamed Ahmed Zaki¹Ahmad F. El-Adawy¹Oliver Flouty⁵Mohamed Hamed¹

• ¹Department of Neurology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
• ²Alexandria Faculty of Medicine, Alexandria University, Alexandria, Egypt
• ³Faculty of Medicine, Hashemite University, Zarqa, Jordan
• ⁴Kasr Alainy Faculty of Medicine, Cairo University, Cairo, Egypt
• ⁵Department of Neurosurgery and Brain Repair, University of South Florida, Tampa, FL, United States

Background: Cerebrovascular diseases of the brain are usually defined by transient ischemic attacks and strokes. However, they can also cause brain injuries without neurological events. Silent brain infarcts (SBI) and leukoaraiosis are symptoms of both vascular and neurological abnormalities. This study aims to investigate the association between SBI, leukoaraiosis, and middle-aged patients with ischemic stroke.

Methods: A single-center retrospective study of 50 middle-aged, ischemic stroke patients were studied from November 2022 and May 2023. The patients were divided into two groups based on the presence or absence of leukoaraiosis. History taking, physical examination, brain CT scan, and MRI were all part of the diagnostic process. Metabolic syndrome (MetS) was also assessed through various factors. The statistical analysis included descriptive statistics, logistic regression analysis, and chi-square test.

Results: Out of the cohort comprising 50 patients, characterized by a mean age of 52.26 years (SD 5.29), 32 were male, constituting 64% of the sample. Among these patients, 26 individuals exhibited leukoaraiosis, with 17 of them (65.4%) also presenting with SBI. Moreover, within this cohort, 22 patients were diagnosed with MetS, representing 84.6% of those affected. The Multivariate logistic regression analysis showed a strong and independent association between leukoaraiosis and SBI. Individuals with leukoaraiosis were nearly five times more likely to have SBI compared to those without leukoaraiosis.

Conclusion: The study highlights leukoaraiosis as a significant risk factor for SBI, alongside MetS. Advanced imaging techniques have facilitated their detection, revealing a higher prevalence among stroke patients, particularly associated with age and hypertension. Further research is needed to fully understand their complex relationship and develop better management strategies for cerebrovascular diseases, ultimately improving patient outcomes.

Introduction

Historically, cerebrovascular disease of the brain has been defined by the symptoms and signs of transient ischemic attack or stroke. However, neuropathological studies in highly selected populations have revealed that vascular disease can cause brain injury in the absence of these acute neurological events. The advent of advanced brain-imaging techniques, such as computerized tomography (CT) and Magnetic resonance imaging (MRI), has allowed similar observations to be made in patient groups and healthy individuals, necessitating a reconsideration of the definition of cerebrovascular disease (1, 2). Signs of cerebral small vessel disease on conventional MRI include leukoaraiosis, recent subcortical lacunar infarcts (clinically symptomatic), lacunes (clinically silent), cerebral microbleeds, prominent perivascular spaces, and cerebral atrophy (3). These brain infarcts, while often asymptomatic, demand increased attention to mitigate the deleterious effects of vascular disease in the brain. Silent brain infarctions (SBIs) comprise two subtypes: lacunar and non-lacunar, resulting from small perforating artery occlusion and embolism or athero-sclerotic stenosis, respectively. The advancement of MRI technology enables the distinction between these subtypes (4–6). Therefore, exploring the distinct risk factors between the two subtypes, especially in the case of SBI, could lead to the development of specific prevention strategies, particularly for middle-aged individuals. Hypertension (HTN), apart from age, is the most widely accepted risk factor associated with SBI. Furthermore, the consistent correlation between hypertension and these infarcts suggests a critical role for hypertensive small-vessel disease in their pathogenesis (7). However, further research is necessary to better define the association between hypertension and brain infarcts, particularly in terms of preventing SBI through effective hypertension control. SBI and leukoaraiosis (LA) are intricate cerebral manifestations that have garnered considerable attention due to their association with diverse vascular and metabolic abnormalities. Hence, comprehending the intricate relationship between these cerebral alterations and MetS is of paramount importance for elucidating their underlying mechanisms and devising effective prevention and management strategies. Leukoaraiosis was observed through MRI and manifests as increased signal intensity in the white matter, often attributed to small vessel disease and pathological processes such as demyelination, gliosis, and vessel lipo hyalinosis (8). Conversely, SBIs denote brain tissue damage resulting from inadequate blood supply without acute neurological symptoms. Though often asymptomatic, SBIs pose a substantial risk for future stroke and cognitive decline (9). MetS plays a pivotal role in the development of LA and SBIs, operating through mechanisms such as vascular dysfunction, inflammation, insulin resistance, and dyslipidemia (10). The diagnosis of LA and SBIs primarily relies on MRI techniques, with fluid-attenuated inversion recovery (FLAIR) imaging sequences commonly employed to detect and assess the extent of white matter changes (11). Epidemiological data indicate a higher prevalence of LA and SBIs with advancing age, affecting a significant proportion of individuals over 65 years. This research aims to investigate the association between LA, SBIs, and middle-aged patients with ischemic stroke. The study focuses on middle-aged stroke patients to address the critical period in stroke epidemiology, capture a substantial portion of stroke cases in a relatively younger age group, identify early risk factors and pathophysiological mechanisms, and provide clinically relevant insights for healthcare providers in terms of risk stratification, diagnostics, and treatment strategies.

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