Frequency of silent brain lesions and aspirin protection evaluation over 3 years follow-up in beta thalassemia patients.

Silent brain lesions might be associated with overt cerebrovascular accident over time in beta thalassemia major (BTM) and intermediate (BTI). Aspirin may be protective in these patients. We evaluated brain magnetic resonance imaging (MRI) in thalassemia patients to see whether aspirin is protective or not. A historical cohort study was conducted on 35 thalassemia patients, 22 BTI, and 13 BTM patients at Shiraz Hematology Research Center in 2018. Median age of the patients was 32 years and ranged from 8 to 42 years. Twenty-four patients (68.6%) were females. Overall frequency of white matter lesions (WMLs) in the first MRI was 10 patients (28.6%). After 3 years, 3 patients developed new lesions and the frequency of WMLs was 13 patients (37.1%) in the second MRI. Moreover, in 3 patients, number of WMLs increased. Patients with new lesions or more lesions compared to the baseline were significantly older than the other group (median age 36.5 years vs. 31 years, P = 0.046). Regarding aspirin consumption, only 1 patient (16.7%) of patients with new lesions was using aspirin compared to 10 (34.5%) of the other group (P = 0.640). The high-risk patients with thrombocytosis, splenectomy, severe iron overload, and older age (> 30 years) should be under close follow-up and evaluated on a regular periodic basis as well as brain MRI at least once every 3 years. Aspirin could be protective against new or progressive brain lesions so that low-dose aspirin is recommended in high-risk thalassemia patients.

C-reactive protein levels are associated with cerebral small vessel-related lesions.

OBJECTIVE: Inflammation has received increasing attention as a cause of stroke. Although several lines of evidence suggest that inflammatory processes have a role in arteriosclerotic vascular events, their involvement remains to be determined. The purpose of this study was to examine the associations between serum high-sensitive C-reactive protein (hs-CRP) levels and cerebral small vessel (CSV)-related lesions as a manifestation of arteriosclerosis. MATERIALS AND METHODS: Neurologically normal subjects without any history of neurologic or psychiatric diseases were enrolled (n = 519). All the participants underwent magnetic resonance imaging (MRI), and their CSV-related lesions (i.e., lacunar infarcts, cerebral microbleeds, deep white matter hyperintensity, and periventricular hyperintensity) were evaluated. The serum levels of hs-CRP were evaluated as common inflammatory markers. RESULTS: Subjects with higher C-reactive protein (CRP) levels had more lacunar infarcts (P = 0.02). After adjusting for the traditional cardiovascular risk factors, higher hs-CRP levels were still associated with the presence of lacunar infarcts [odds ratio for the highest vs the lowest tertile of hs-CRP, 3.57 (95% confidence interval: 1.30-9.80)]. These associations did not change when the logarithmically transformed values for hs-CRP were included. Furthermore, subjects with higher CRP levels had more cerebral microbleeds (P = 0.03), more severe deep white matter hyperintensity (P = 0.04), and periventricular hyperintensity (P = 0.04); however, these associations were not observed after adjusting for the cardiovascular risk factors. CONCLUSIONS: Higher levels of hs-CRP were associated with lacunar infarcts. Thus, inflammatory processes may be involved in the pathogenesis of small-vessel disease.

Right-to-Left Shunt in Divers with Neurological Decompression Sickness: A Systematic Review and Meta-Analysis.

OBJECTIVE: The aim of this study was to assess the association between the presence of a right-to-left shunt (RLS) and neurological decompression sickness (NDCS) and asymptomatic brain lesions among otherwise healthy divers. BACKGROUND: Next to drowning, NDCS is the most severe phenotype of diving-related disease and may cause permanent damage to the brain and spinal cord. Several observational reports have described the presence of an RLS as a significant risk factor for neurological complications in divers, ranging from asymptomatic brain lesions to NDCS. METHODS: We systematically reviewed the MEDLINE, Embase, and CENTRAL databases from inception until November 2021. A random-effects model was used to compute odds ratios. RESULTS: Nine observational studies consisting of 1830 divers (neurological DCS: 954; healthy divers: 876) were included. RLS was significantly more prevalent in divers with NDCS compared to those without (62.6% vs. 27.3%; odds ratio (OR): 3.83; 95% CI: 2.79-5.27). Regarding RLS size, high-grade RLS was more prevalent in the NDCS group than the no NDCS group (57.8% versus 18.4%; OR: 4.98; 95% CI: 2.86-8.67). Further subgroup analysis revealed a stronger association with the inner ear (OR: 12.13; 95% CI: 8.10-18.17) compared to cerebral (OR: 4.96; 95% CI: 2.43-10.12) and spinal cord (OR: 2.47; 95% CI: 2.74-7.42) DCS. RLS was more prevalent in divers with asymptomatic ischemic brain lesions than those without any lesions (46.0% vs. 38.0%); however, this was not statistically significant (OR: 1.53; 95% CI: 0.80-2.91). CONCLUSIONS: RLS, particularly high-grade RLS, is associated with greater risk of NDCS. No statistically significant association between RLS and asymptomatic brain lesions was found.

Incidence and impact of silent brain lesions after coronary artery bypass grafting.

OBJECTIVE: Silent brain lesions are known to occur after coronary artery bypass grafting (CABG). The aim of this study was to seek the incidence rate, the influence of procedures, and their impact on the postoperative course. METHODS: From July 2016 to April 2018, 104 consecutive patients undergoing elective and isolated first-time CABG (65 off-pump and 39 on-pump) were enrolled. New brain lesions were evaluated by brain magnetic resonance imaging both before and after CABG. Postoperative outcomes, including cognitive function, were compared between patients with and without brain lesions. RESULTS: The overall incidence of new brain lesions was 20.1% (21/104). Excluding one symptomatic stroke case, silent brain lesions were revealed in the remaining patients. The percentage of on-pump CABG (61.9% [13/21] vs 31.3% [26/83], P = .019) and aortic clamp (52.4% [11/21] vs 24.1% [20/83], P = .014) were significantly greater in patients with brain lesions. Brain lesions were observed in 12.3% and 15.8% of patients in the off-pump and anaortic CABG. The Katz Index of Independence in Activities of Daily Living was significantly lower in patients with brain lesions (from 5.8 ± 0.9 to 5.4 ± 1.2 vs from 5.9 ± 0.5 to 5.9 ± 0.6, P = .013). In patients with new lesions, postoperative cognitive dysfunction (POCD) was observed only in multiple lesions, and the maximum size was significantly greater in patients with POCD. CONCLUSIONS: Magnetic resonance imaging of the brain frequently detected postoperative silent brain lesions after CABG in off-pump and aorta non-touch groups. Multiple and larger new brain lesions were associated with the development of POCD.

Serial Magnetic Resonance Imaging after Electrical Cardioversion of Recent Onset Atrial Fibrillation in Anticoagulant-Naïve Patients - A Prospective Study Exploring Clinically Silent Cerebral Lesions.

BACKGROUND: Patients with atrial fibrillation (AF) have a high incidence of cognitive impairment, which may be related to clinically silent microembolism causing cerebral infarctions. OBJECTIVE: To explore the occurrence and timing of silent brain lesions following electrical cardioversion (CV) of recent onset AF in anticoagulant-naïve patients and to study related effects on cognitive function and biomarkers of cerebral damage, S100b. METHODS: Patients with AF duration > 48 hours were prospectively included. Brain magnetic resonance imaging (MRI) and S100b, were obtained prior, after and 7-10 days following CV. Trail making tests (TMT-A and TMT-B) and their difference, ΔΤΜΤ, were assessed prior to CV, 7-10 days and 30 days after CV. RESULTS: Forty-three patients (84% males) with median CHA2DS2-VASc score 1 (interquartile range 0-1) were included. Sequential MRI, including diffusion weighted scans, showed no new brain lesions after CV. Chronic white matter hyperintensities were present at baseline in 21/43 (49%) patients. The S100b (µg/l) levels increased significantly from baseline, (mean ±SD) 0.0472±0.0182 to 0.0551±0.0185 after CV, p=0.001 and then decreased 7-10 days after CV to 0.0450±0.0186, p <.;0.001. Consecutive TMT scores improved successively after CV, being statistically and clinically significant for TMT-B (p<0.01) and ΔΤΜΤ (p=0.005) between 7-10 days and 30 days after CV (Reliable Change Index >1.96). CONCLUSIONS: New brain lesions could not be detected on MRI after CV, but the high incidence of white matter hyperintensities and the transient increase in S100b may indicate transient or minor brain damage undetectable by MRI thus heightening the need to reevaluate thromboembolic risk prior to CV even in low risk patients.

Silent New Brain Lesions: Innocent Bystander or Guilty Party?

With the advances in magnetic resonance imaging, previously unrecognized small brain lesions, which are mostly asymptomatic, have been increasingly detected. Diffusion-weighted imaging can identify small ischemic strokes, while gradient echo T2* imaging and susceptibility-weighted imaging can reveal tiny hemorrhagic strokes (microbleeds). In this article, we review silent brain lesions appearing soon after acute stroke events, including silent new ischemic lesions and microbleeds appearing 1) after acute ischemic stroke and 2) after acute intracerebral hemorrhage. Moreover, we briefly discuss the clinical implications of these silent new brain lesions.

Association of mild kidney dysfunction with silent brain lesions in neurologically normal subjects.

BACKGROUND: Chronic kidney disease (CKD) has been closely associated with stroke. Although a large number of studies reported the relationship between CKD and different types of asymptomatic brain lesions, few comprehensive analyses have been performed for all types of silent brain lesions. METHODS: We performed a cross-sectional study involving 1,937 neurologically normal subjects (mean age 59.4 years). Mild CKD was defined as an estimated glomerular filtration rate between 30 and 60 ml/min/1.73 m(2) or positive proteinuria. RESULTS: The prevalence of mild CKD was 8.7%. Univariate analysis revealed an association between CKD and all silent brain lesions, including silent brain infarction, periventricular hyperintensity, subcortical white matter lesion, and microbleeds, in addition to hypertension and diabetes mellitus after adjusting for age and sex. In binary logistic regression analysis, the presence of CKD was a significant risk factor for all types of silent brain lesions, independent of other risk factors. CONCLUSIONS: These results suggest that mild CKD is independently associated with all types of silent brain lesions, even in neurologically normal subjects.

Silent New Brain Lesions: Innocent Bystander or Guilty Party? / 대한뇌졸중학회지

With the advances in magnetic resonance imaging, previously unrecognized small brain lesions, which are mostly asymptomatic, have been increasingly detected. Diffusion-weighted imaging can identify small ischemic strokes, while gradient echo T2* imaging and susceptibility-weighted imaging can reveal tiny hemorrhagic strokes (microbleeds). In this article, we review silent brain lesions appearing soon after acute stroke events, including silent new ischemic lesions and microbleeds appearing 1) after acute ischemic stroke and 2) after acute intracerebral hemorrhage. Moreover, we briefly discuss the clinical implications of these silent new brain lesions.

Silent New Brain Lesions: Innocent Bystander or Guilty Party? / 대한뇌졸중학회지

With the advances in magnetic resonance imaging, previously unrecognized small brain lesions, which are mostly asymptomatic, have been increasingly detected. Diffusion-weighted imaging can identify small ischemic strokes, while gradient echo T2* imaging and susceptibility-weighted imaging can reveal tiny hemorrhagic strokes (microbleeds). In this article, we review silent brain lesions appearing soon after acute stroke events, including silent new ischemic lesions and microbleeds appearing 1) after acute ischemic stroke and 2) after acute intracerebral hemorrhage. Moreover, we briefly discuss the clinical implications of these silent new brain lesions.