The guardian of intracranial vessels: Why the pericyte?

Intracranial atherosclerotic stenosis (ICAS) is a pathological condition characterized by progressive narrowing or complete blockage of intracranial blood vessels caused by plaque formation. This condition leads to reduced blood flow to the brain, resulting in cerebral ischemia and hypoxia. Ischemic stroke (IS) resulting from ICAS poses a significant global public health challenge, especially among East Asian populations. However, the underlying causes of the notable variations in prevalence among diverse populations, as well as the most effective strategies for preventing and treating the rupture and blockage of intracranial plaques, remain incompletely comprehended. Rupture of plaques, bleeding, and thrombosis serve as precipitating factors in the pathogenesis of luminal obstruction in intracranial arteries. Pericytes play a crucial role in the structure and function of blood vessels and face significant challenges in regulating the Vasa Vasorum (VV)and preventing intraplaque hemorrhage (IPH). This review aims to explore innovative therapeutic strategies that target the pathophysiological mechanisms of vulnerable plaques by modulating pericyte biological function. It also discusses the potential applications of pericytes in central nervous system (CNS) diseases and their prospects as a therapeutic intervention in the field of biological tissue engineering regeneration.

Global intracranial arterial tortuosity is associated with intracranial atherosclerotic burden.

The effect of arterial tortuosity on intracranial atherosclerosis (ICAS) is not well understood. This study aimed to evaluate the effect of global intracranial arterial tortuosity on intracranial atherosclerotic burden in patients with ischemic stroke. We included patients with acute ischemic stroke who underwent magnetic resonance angiography (MRA) and classified them into three groups according to the ICAS burden. Global tortuosity index (GTI) was defined as the standardized mean curvature of the entire intracranial arteries, measured by in-house vessel analysis software. Of the 516 patients included, 274 patients had no ICAS, 140 patients had a low ICAS burden, and 102 patients had a high ICAS burden. GTI increased with higher ICAS burden. After adjustment for age, sex, vascular risk factors, and standardized mean arterial area, GTI was independently associated with ICAS burden (adjusted odds ratio [adjusted OR] 1.33; 95% confidence interval [CI] 1.09-1.62). The degree of association increased when the arterial tortuosity was analyzed limited to the basal arteries (adjusted OR 1.48; 95% CI 1.22-1.81). We demonstrated that GTI is associated with ICAS burden in patients with ischemic stroke, suggesting a role for global arterial tortuosity in ICAS.

Delayed Enhancement of Intracranial Atherosclerotic Plaque Can Better Differentiate Culprit Lesions: A Multiphase Contrast-Enhanced Vessel Wall MRI Study.

BACKGROUND AND PURPOSE: Intracranial plaque enhancement (IPE) identified by contrast-enhanced vessel wall MR imaging (VW-MR imaging) is an emerging marker of plaque instability related to stroke risk, but there was no standardized timing for postcontrast acquisition. We aim to explore the optimal postcontrast timing by using multiphase contrast-enhanced VW-MR imaging and to test its performance in differentiating culprit and nonculprit lesions. MATERIALS AND METHODS: Patients with acute ischemic stroke due to intracranial plaque were prospectively recruited to undergo VW-MR imaging with 1 precontrast phase and 4 consecutive postcontrast phases (9 minutes and 13 seconds for each phase). The signal intensity (SI) values of the CSF and intracranial plaque were measured on 1 precontrast and 4 postcontrast phases to determine the intracranial plaque enhancement index (PEI). The dynamic changes of the PEI were compared between culprit and nonculprit plaques on the postcontrast acquisitions. RESULTS: Thirty patients with acute stroke (aged 59 ± 10 years, 18 [60%] men) with 113 intracranial plaques were included. The average PEI of all intracranial plaques significantly increased (up to 14%) over the 4 phases. There was significantly increased PEI over the 4 phases for culprit plaques (an average increase of 23%), but this was not observed for nonculprit plaques. For differentiating culprit and nonculprit plaques, we observed that the performance of IPE in the second postcontrast phase (cutoff = 0.83, AUC = 0.829 [0.746-0.893]) exhibited superior accuracy when compared with PEI in the first postcontrast phase (cutoff = 0.48; AUC = 0.768 [0.680-0.843]) (P = .022). CONCLUSIONS: A 9-minute delay of postcontrast acquisition can maximize plaque enhancement and better differentiate between culprit and nonculprit plaques. In addition, culprit and nonculprit plaques have different enhancement temporal patterns, which should be evaluated in future studies.

Carotid atherosclerotic plaque predicts progression of intracranial artery atherosclerosis: A MR imaging-based community cohort study.

PURPOSE: Intracranial artery atherosclerosis (ICAS) progression is associated with stroke. However, the association of carotid plaque with ICAS progression among stroke-free participants is still unclear. This study aimed to evaluate the association between carotid plaque and ICAS progression in stroke-free participants. METHOD: Stroke-free participants were recruited from a community-based cohort study. All participants underwent questionnaire interviews, blood tests, and high-resolution vessel wall magnetic resonance (MR) imaging at baseline and follow-up for around three years. The atherosclerotic plaque was defined as eccentric wall thickening on MR imaging. The presence, location, total number, and burden (maximum wall thickness, length, and stenosis) of carotid and intracranial plaque were evaluated. ICAS progression was defined as the number increased or plaque burden (maximum wall thickness, length, or stenosis increase) increased by ≥ 20 %. The association between carotid plaque and ICAS progression was evaluated using multivariable logistic regression. RESULTS: Of the 312 participants (mean age at baseline: 59.85 ± 13.04 years; 136 males) who completed baseline and follow-up studies with a mean time interval of 3.15 ± 0.59 years, 85 (27.24 %) had progression of ICAS during follow-up. At least one carotid plaque was detected at baseline in 167 (53.53 %) participants. In the multivariable logistic analysis, carotid plaque was a significant predictor for the progression of ICAS (odds ratio, 2.04; 95 % confidence interval, 1.06-3.92; P = 0.032). CONCLUSIONS: Carotid plaque is associated with intracranial artery atherosclerosis progression in stroke-free population. Our findings suggest that carotid plaque may be an effective predictor for intracranial artery atherosclerosis progression.

Association of systemic inflammatory response index and plaque characteristics with the severity and recurrence of cerebral ischemic events.

AIM: We aimed to investigate the relationship between systemic inflammatory response index (SIRI) and intracranial plaque features, as well as the risk factors related to the severity and recurrence of cerebral ischemic events. METHODS: We enrolled 170 patients with cerebral ischemic events. Baseline demographic characteristics and laboratory indicators were collected from all participants. All patients were assessed by high-resolution magnetic resonance vessel wall imaging for culprit plaque characteristics and intracranial atherosclerotic burden. Outpatient or telephone follow-up were conducted at 1, 3, and 6 months after discharge. RESULTS: SIRI levels were significantly associated with the enhanced plaque number (r = 0.205, p = 0.007), total plaque stenosis score (r = 0.178, p = 0.020), total plaque enhancement score (r = 0.222, p = 0.004), intraplaque hemorrhage (F = 5.630, p = 0.004), and plaque surface irregularity (F = 3.986, p = 0.021). Higher SIRI levels (OR = 1.892), total plaque enhancement score (OR = 1.392), intraplaque hemorrhage (OR = 3.370) and plaque surface irregularity (OR = 2.846) were independent risk factors for moderate-severe stroke, and these variables were significantly positively correlated with NIHSS (P < 0.05 for all). In addition, higher age (HR = 1.063, P = 0.015), higher SIRI levels (HR = 2.003, P < 0.001), and intraplaque hemorrhage (HR = 4.482, P = 0.008) were independently associated with recurrent stroke. CONCLUSIONS: Higher SIRI levels may have adverse effects on the vulnerability and burden of intracranial plaques, and links to the severity and recurrence of ischemic events. Therefore, SIRI may provide important supplementary information for evaluating intracranial plaque stability and risk stratification of patients.

Width of sulcus and thickness of gyrus in patients with cerebral atherosclerosis: a new tool for the prevention of vascular cognitive impairment

SUMMARY BACKGROUND AND PURPOSE Cerebral atherosclerosis is the main cause of lesions that contribute to vascular cognitive impairment and vascular dementia, followed by arteriosclerosis of small vessels and cerebral amyloid angiopathy. The purpose of this study was to compare the post-mortem radiological alterations of autopsied adults with the macroscopic alterations in the posterior region of these brains in order to establish a relationship between the two forms of analysis and to discuss the relevance of the prevention of vascular cognitive impairment in patients with encephalic atherosclerosis. MATERIALS AND METHODS Thirteen brains were analysed macroscopically to assess the degree of atherosclerosis of the basilar and the posterior cerebral arteries. The patients were autopsied in the Subject of General Pathology at General Hospital of Triângulo Mineiro Federal University in Uberaba, state of Minas Gerais, Brazil. The qualitative analysis of atherosclerosis was performed with classification into mild, moderate or severe. In the posterior region of the brains, width of sulcus and thickness of gyrus were measured by macroscopic analysis and by tomographic analysis. RESULTS AND CONCLUSIONS There was a decrease in calcarine sulcus width and an increase in medial temporal occipital gyrus thickness in patients with a higher degree of atherosclerosis, macroscopically and in tomography, respectively. Low oxygenation caused by atherosclerosis probably leads to an encephalic parenchyma inflammation that causes microglial cells hypertrophy provoking increase in the gyrus thickness and decrease in the sulcus width, as observed in the present study.

RESUMO INTRODUÇÃO E OBJETIVO A aterosclerose cerebral é a principal causa de lesões que contribuem para o comprometimento cognitivo vascular (CCV) e demência vascular, seguida da arteriosclerose de pequenos vasos e da angiopatia amiloide cerebral. Sendo assim, este estudo comparou as alterações radiológicas post mortem de adultos autopsiados com as alterações macroscópicas na região posterior desses encéfalos a fim de estabelecer uma relação entre as duas formas de análise e discutir sobre a relevância da prevenção do CCV em pacientes com aterosclerose encefálica. MATERIAL E MÉTODOS Treze encéfalos foram analisados macroscopicamente para avaliar o grau de aterosclerose das artérias basilar e cerebral posterior. Os pacientes foram autopsiados na disciplina de Patologia Geral no HC-UFTM em Uberaba, Minas Gerais, Brasil. A análise qualitativa da aterosclerose foi realizada com as classificações discreta, moderada ou acentuada. A espessura dos giros e a largura dos sulcos na região posterior dos encéfalos foram analisadas macroscopicamente e por tomografia computadorizada. RESULTADOS E CONCLUSÃO Houve diminuição na largura do sulco calcarino e aumento na espessura do giro occipital temporal medial de acordo com o aumento do grau de aterosclerose macroscopicamente e por tomografia, respectivamente. A baixa oxigenação causada pela aterosclerose provoca a inflamação do parênquima encefálico, provavelmente levando à hipertrofia das células da micróglia e ao consequente aumento dos giros e estreitamento dos sulcos, como observado no presente estudo.

Enfermedad de Binswanger: evolucion de las ideas y propuesta de un tripode diagnóstico / Binswanger's disease: thought's evolution and a proposal of diagnostic triad

Estudamos a evoluçäo do conceito de doença de Binswanger a partir de 1894, ano de sua descriçäo inicial. Observamos que, posteriormente a uma fase com escassos relatos, com a introduçäo da tomografia computadorizada de crânio, há uma fase de sobrediagnóstico e de perda dos conceitos básicos, levando a confusäo na literatura. Propomos a utilizaçäo de um tripé diagnóstico - clínico, radiológico e anátomo-patológico - que ajudará o correto posicionamento médico perante essa doença