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Cephalosporin is widely used in clinical practice due to its broad anti-bacterial activity. However, some serious side effects have been reported. Here, we report a 79-year-old male who repeatedly experienced toxic encephalopathy after consecutive administration of third and first generation cephalosporins. This case demonstrated that various type of cephalosporin may cause toxic encephalopathy and emphasized the importance of staying vigilance for the rare but potentially curable side effects of one of the most widely prescribed antibiotics.

Background and ObjectivesFemale patients tend to have greater disability and worse long-term outcomes after stroke than male patients. To date, the biological basis of sex difference in ischemic stroke remains unclear. We aimed to 1) assess sex differences in clinical manifestation and outcomes of acute ischemic stroke and 2) investigate whether the sex disparity is due to different infarct locations or different impacts of infarct in the same location.MethodsThis MRI-based multicenter study included 6,464 consecutive patients with acute ischemic stroke (ResultsMean (SD) age was 67.5 (12.6) years, and 2,641 (40.9%) were female patients. Percentage infarct volumes on diffusion-weighted MRI did not differ between female patients and male patients (median 0.14% vs. 0.14%, P=0.35). However, female patients showed higher stroke severity (NIHSS-score, median 4 vs. 3, P2) than male patients (adjusted-absolute-difference 4.5%; 95%-CI 2.0–7.0; PDiscussionFemale patients have more frequent middle cerebral artery disease and striatocapsular motor-pathway involvement with acute ischemic stroke, along with left parieto-occipital cortical infarcts showing greater severity for equivalent infarct volumes than in male patients. This leads to more severe initial neurological symptoms, higher susceptibility to neurological worsening, and less 3-month functional independence, when compared with male patients.

Atypical psychological symptoms frequently occur in early-onset Alzheimer’s disease (EOAD), which makes it difficult to differentiate it from other psychiatric disorders. We report the case of a 28-year-old woman with EOAD, carrying a presenilin-1 mutation (S170P), who was initially misdiagnosed with schizophrenia because of prominent psychiatric symptoms in the first 1–2 years of the disease. Amyloid-β positron emission tomography (PET) showed remarkably high tracer uptake in the striatum and thalamus. Tau PET showed widespread cortical uptake and relatively low uptake in the subcortical and medial temporal regions. Our case advocates for considering EOAD diagnosis for young patients with psychiatric and atypical cognitive symptoms.

ImportancePolygenic risk scores (PRSs), which aggregate the genetic effects of single-nucleotide variants identified in genome-wide association studies (GWASs), can help distinguish individuals at a high genetic risk for Alzheimer disease (AD). However, genetic studies have predominantly focused on populations of European ancestry.ObjectiveTo evaluate the transferability of a PRS for AD in the Korean population using summary statistics from a prior GWAS of European populations.Design, Setting, and ParticipantsThis cohort study developed a PRS based on the summary statistics of a large-scale GWAS of a European population (the International Genomics of Alzheimer Project; 21 982 AD cases and 41 944 controls). This PRS was tested for an association with AD dementia and its related phenotypes in 1634 Korean individuals, who were recruited from 2013 to 2019. The association of a PRS based on a GWAS of a Japanese population (the National Center for Geriatrics and Gerontology; 3962 AD cases and 4074 controls) and a transancestry meta-analysis of European and Japanese GWASs was also evaluated. Data were analyzed from December 2020 to June 2021.Main Outcomes and MeasuresRisk of AD dementia, amnestic mild cognitive impairment (aMCI), earlier symptom onset, and amyloid β deposition (Aβ).ResultsA total of 1634 Korean patients (969 women [59.3%]), including 716 individuals (43.6%) with AD dementia, 222 (13.6%) with aMCI, and 699 (42.8%) cognitively unimpaired controls, were analyzed in this study. The mean (SD) age of the participants was 71.6 (9.0) years. Higher PRS was associated with a higher risk of AD dementia independent of APOE ɛ4 status in the Korean population (OR, 1.95; 95% CI, 1.40-2.72; P APOE ɛ4 status. The PRS based on a transancestry meta-analysis of data sets comprising 2 distinct ancestries showed a slightly improved accuracy.Conclusions and RelevanceIn this cohort study, a PRS derived from a European GWAS identified individuals at a high risk for AD dementia in the Korean population. These findings emphasize the transancestry transferability and clinical value of PRSs and suggest the importance of enriching diversity in genetic studies of AD.

Background: Primary progressive aphasia (PPA) is associated with amyloid-β (Aβ) pathology. However, clinical feature of PPA based on Aβ positivity remains unclear. Objective: We aimed to assess the prevalence of Aβ positivity in patients with PPA and compare the clinical characteristics of patients with Aβ-positive (A+) and Aβ-negative (A–) PPA. Further, we applied Aβ and tau classification system (AT system) in patients with PPA for whom additional information of in vivo tau biomarker was available. Methods: We recruited 110 patients with PPA (41 semantic [svPPA], 27 non-fluent [nfvPPA], 32 logopenic [lvPPA], and 10 unclassified [ucPPA]) who underwent Aβ-PET imaging at multi centers. The extent of language impairment and cortical atrophy were compared between the A+ and A–PPA subgroups using general linear models. Results: The prevalence of Aβ positivity was highest in patients with lvPPA (81.3%), followed by ucPPA (60.0%), nfvPPA (18.5%), and svPPA (9.8%). The A+ PPA subgroup manifested cortical atrophy mainly in the left superior temporal/inferior parietal regions and had lower repetition scores compared to the A–PPA subgroup. Further, we observed that more than 90% (13/14) of the patients with A+ PPA had tau deposition. Conclusion: Our findings will help clinicians understand the patterns of language impairment and cortical atrophy in patients with PPA based on Aβ deposition. Considering that most of the A+ PPA patents are tau positive, understanding the influence of Alzheimer’s disease biomarkers on PPA might provide an opportunity for these patients to participate in clinical trials aimed for treating atypical Alzheimer’s disease.

Background: An association between Helicobacter pylori (H. pylori) infection and dementia was reported in previous studies; however, the evidence is inconsistent. Objective: In the present study, the association between H. pylori infection and brain cortical thickness as a biomarker of neurodegeneration was investigated. Methods: A cross-sectional study of 822 men who underwent a medical health check-up, including an esophagogastroduodenoscopy and 3.0 T magnetic resonance imaging, was performed. H. pylori infection status was assessed based on histology. Multiple linear regression analyses were conducted to evaluate the relationship between H. pylori infection and brain cortical thickness. Results: Men with H. pylori infection exhibited overall brain cortical thinning (p = 0.022), especially in the parietal (p = 0.008) and occipital lobes (p = 0.050) compared with non-infected men after adjusting for age, educational level, alcohol intake, smoking status, and intracranial volume. 3-dimentional topographical analysis showed that H. pylori infected men had cortical thinning in the bilateral lateral temporal, lateral frontal, and right occipital areas compared with non-infected men with the same adjustments (false discovery rate corrected, Q

Tau and amyloid β (Aβ), 2 key pathogenic proteins in Alzheimer’s disease (AD), reportedly spread throughout the brain as the disease progresses. Models of how these pathogenic proteins spread from affected to unaffected areas had been proposed based on the observation that these proteins could transmit to other regions either through neural fibers (transneuronal spread model) or through extracellular space (local spread model). In this study, we modeled the spread of tau and Aβ using a graph theoretical approach based on resting-state functional magnetic resonance imaging. We tested whether these models predict the distribution of tau and Aβ in the brains of AD spectrum patients. To assess the models’ performance, we calculated spatial correlation between the model-predicted map and the actual map from tau and amyloid positron emission tomography. The transneuronal spread model predicted the distribution of tau and Aβ deposition with significantly higher accuracy than the local spread model. Compared with tau, the local spread model also predicted a comparable portion of Aβ deposition. These findings provide evidence of transneuronal spread of AD pathogenic proteins in a large-scale brain network and furthermore suggest different contributions of spread models for tau and Aβ in AD.

Additional file 1: Table S1. The number of 18F-flutemetamol uptake regions in cognitively unimpaired, amnestic mild cognitive impairment, and Alzheimer's disease dementia at baseline. Fig. S1. Scatter plot and regression line showing a significant correlation between the number of 18F-flutemetamol uptake regions and global SUVR.

ObjectiveTo identify single nucleotide polymorphisms (SNPs) associated with cognitive decline independent of β-amyloid (Aβ) and tau pathology in Alzheimer disease (AD).MethodsDiscovery and replication datasets consisting of 414 individuals (94 cognitively normal control [CN], 185 with mild cognitive impairment [MCI], and 135 with AD) and 72 individuals (22 CN, 39 with MCI, and 11 with AD), respectively, were obtained from the Alzheimer's Disease Neuroimaging Initiative database. Genome-wide association analysis was conducted to identify SNPs associated with individual cognitive function (measured with the Mini-Mental State Examination and Alzheimer's Disease Assessment Scale–Cognitive Subscale ) while controlling for the level of Aβ and tau (measured as CSF phosphorylated-tau/Aβ1-42). Gene ontology analysis was performed on SNP-associated genes.ResultsWe identified 1 significant (rs55906536, β = −1.91, standard error 0.34, p = 4.07 × 10−8) and 4 suggestive variants on chromosome 6 that were associated with poorer cognitive function. Congruent results were found in the replication data. A structural equation model showed that the identified SNP deteriorated cognitive function partially through cortical thinning of the brain in a region-specific manner. Furthermore, a bioinformatics analysis showed that the identified SNPs were associated with genes related to glutathione metabolism.ConclusionsIn this study, we identified SNPs related to cognitive decline in a manner that could not be explained by Aβ and tau levels. Our findings provide insight into the complexity of AD pathogenesis and support the growing literature on the role of glutathione in AD.

Background An association between Helicobacter pylori (H. pylori) infection and dementia was reported in previous studies, however, the evidence is inconsistent. In the present study, the association between H. pylori infection and brain cortical thickness as a biomarker of neurodegeneration was investigated. Methods A cross-sectional study of 1,446 healthy adults who underwent a medical health check-up, including an esophagogastroduodenoscopy and 3.0 T magnetic resonance imaging was performed. H. pylori infection status was assessed based on histology. Multiple linear regression analysis was conducted to evaluate the relationship between H. pylori infection and brain cortical thickness. Results Males with H. pylori infection exhibited cortical thinning in the bilateral lateral temporal, lateral frontal, and right occipital areas compared with non-infected males after controlling for age, educational level, alcohol intake, smoking status, and intracranial volume. The association remained significant after further adjusting for inflammatory marker (C-reactive protein) and metabolic factors (obesity, dyslipidemia, fasting glucose, and blood pressure). However, an association between H. pylori infection and brain cortical thickness was not observed in females. Conclusions The findings indicate H. pylori infection is associated with neurodegenerative changes in cognitive normal males, independent of chronic inflammation or metabolic syndrome.

Introduction A weak association between amyloid β (Aβ) deposition and neurodegeneration biomarkers, such as brain atrophy, has been repeatedly reported in a subset of patients with Alzheimer disease, suggesting individual differences in response to Aβ deposition. Methods Here, we performed a genome-wide interaction study to identify single-nucleotide polymorphism (SNP) that modify the effect of Aβ (measured by F-florbetapir positron emission tomography) on brain atrophy (measured by cortical thickness using magnetic resonance imaging). We used magnetic resonance imaging, positron emission tomography, cerebrospinal fluid, and genetic data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database [discovery cohort, ADNI-GO/2 (n=723) and replication cohort, ADNI-1 (n=129)]. Results We identified a genome-wide suggestive interaction of rs3807779 SNP (β=-0.14, SE=0.029, P=9.08×10) in the discovery cohort. The greater dosage of rs3807779 SNP increased the detrimental effect of Aβ deposition on cortical thickness. In replication analyses, the congruent results were replicated to confirm our findings. Furthermore, rs3807779 SNP augmented the detrimental effect of Aβ deposition on cognitive function. Genetic profiling showed that rs3807779 has chromatin interactions with the promoter region of MAGI2 gene, suggesting its association with MAGI2 expression. Conclusions These findings demonstrate that subjects carrying the rs3807779 SNP are more susceptible to Aβ-related neurodegeneration.

There have been several MR imaging biomarkers of Alzheimer’s disease (AD) for early diagnosis. Cortical mean diffusivity (MD) is one of them for the study of the cortical microstructural change in AD. However, several factors may overshadow the feasibility of MD as AD biomarker. Thus, current study investigated feasible gray matter microstructure biomarker with higher sensitivity for early AD detection. With the aim of facilitating the early detection of AD, the Alzheimer’s Disease Neuroimaging Initiative (ADNI) proposed two stages based on the memory performance: early mild cognitive impairment (EMCI) and late mild cognitive impairment (LMCI). We propose single shell DTI measure, ‘ radiality ’, for early AD biomarker. It is a dot product between cortical surface normal vector and primary diffusion direction, which presumably reflects the fiber orientation within the cortical column. Here, we gathered images from ADNI phase 2 & 3; 78 cognitive normal, 51 EMCI, 34 LMCI, and 39 AD patients. Then, we evaluated cortical thickness (CTh), MD, amount of amyloid and tau accumulations using PET, which are conventional AD biomarkers. Radiality was projected on gray matter surface to compare and validate the changes along other neuroimage biomarkers. Results showed decreased radiality primarily in entorhinal, insula, frontal and temporal cortex as disease progress onward. Especially, radiality could delineate the difference between cognitive normal and EMCI group while other biomarkers could not. We looked into the relationship between the radiality and other biomarkers to validate its pathological evidence in AD. Overall, radiality showed high association with conventional biomarkers. Additional ROI analysis exhibit dynamics of AD related changes as stages onward. In conclusion, radiality in cortical gray matter showed AD specific changes and relevance with other conventional AD biomarkers with higher sensitivity. Besides, it could show group differences in early AD changes from EMCI which show advantage for early diagnosis than using conventional biomarkers. We provide the evidence of structure changes with cognitive impairment and suggest radiality as a sensitive biomarker for early diagnose and progress monitor AD.

Additional file 1: Supplementary Table 1. Demographics of CN amyloid positivity analysis. Supplementary Table 2. Results of cutoff analysis. Supplementary Fig. 1. Comparison of amyloid-negative CN and amyloid-positive CN. Group differences in radiality, cortical thickness, and mean diffusivity from CN amyloid-negative and -positive. Radiality showed a decrease in the postcentral cortex, CTh showed an increase in the lingual cortex, and MD showed a decrease in the postcentral cortex. Color bar indicates p-value interval of 0.05 to 10− 5.

ObjectivesTo investigate which baseline neuropsychological profile predicts the risk of developing dementia in early-stage Parkinson disease (PD).MethodsWe retrospectively reviewed detailed medical records of 350 drug-naive patients with early-stage PD (follow-up >3 years) who underwent a detailed neuropsychological test at initial assessment. Factor analysis was conducted to determine cognitive profiles that yielded 4 cognitive function factors: factor 1, visual memory/visuospatial; factor 2, verbal memory; factor 3, frontal/executive; and factor 4, attention/working memory/language. Subsequently, we assessed the effect of these cognitive function factors on the risk for dementia conversion. We also constructed a nomogram to calculate the risk for developing dementia over a 5-year follow-up period based on these cognitive profiles.ResultsCox regression analysis demonstrated that a higher composite score of factor 1 (hazard ratio [HR] 0.558, 95% confidence interval [CI] 0.427–0.730), factor 2 (HR 0.768, 95% CI 0.596–0.991), and factor 3 (HR 0.425, 95% CI 0.305–0.593) was associated with a lower risk for dementia conversion, while factor 3 had the most predictive power. The nomogram had a fair ability (Heagerty integrated area under the curve 0.763) to estimate the risk for dementia conversion within 5 years. The composite scores of factor 3 contributed more to the occurrence of dementia in PD than those of the other cognitive function factors.ConclusionsThese findings suggest that these factor analysis–derived cognitive profiles can be used to predict dementia conversion in early-stage PD. In addition, frontal/executive dysfunction contributes most to the occurrence of dementia in PD.

Background Supernumerary phantom limb (SPL) is a rare neurologic phenomenon, in which a patient misperceives an extra limb in addition to the original set of limbs. We report a case of SPL in a patient with a right basal ganglia hemorrhage and review the previous literature about this peculiar phenomenon. Case presentation Two days after the event of a right basal ganglia hemorrhage, a 78-year-old male reported a phantom arm protruding from his left shoulder. He could not see or touch the phantom arm but he felt the presence of an addition arm lateral to his paretic arm. Pain or sensory discomfort were absent in either the paretic arm or the phantom arm. He stated that he could intentionally move the phantom arm independent of his paretic arm. The examination showed that the passive movement of his paretic arm did not elicit any movement of his phantom arm. We diagnosed the SPL as a complication of the hypertensive basal ganglia hemorrhage and treated him with anti-hypertensive medications. His phantom arm persisted for 3 weeks, and it gradually faded away. Conclusion SPL had been reported as a rare complication of various types of cerebral lesions. Right hemispheric lesions were most frequently associated with the SPL. Considering the intentional movement of the phantom arm, we deduced that the SPL might result from the impairment of the sensory feedback system for both internal body image and motor movement.

Metabolic syndrome is a cluster of metabolic abnormalities including obesity, hypertension, hypertriglyceridemia, low high-density lipoprotein cholesterol, and hyperglycemia. Obstructive sleep apnea (OSA) is known to be associated with metabolic syndrome. However, it remains uncertain which sleep parameters of OSA are associated with metabolic syndrome. We aimed to clarify the relationship between sleep variables and the presence of metabolic syndrome in patients with OSA. We prospectively recruited patients who visited the institute for the evaluation of sleep-disordered breathing. All patients underwent overnight polysomnography and sleep questionnaires. They were diagnosed with metabolic syndrome according to the 2007 consensus definition by the International Diabetes Federation. We applied multivariate logistic regression models to predict the presence of metabolic syndrome with variables related to sleep parameters. A total of 85 patients (43 men) were enrolled. The mean age (± standard deviation) was 52.0 ± 14.3 years. Metabolic syndrome was diagnosed in 39 (46%) patients. Patients with metabolic syndrome had a significantly higher apnea-hypopnea index (AHI) compared with patients without metabolic syndrome. An AHI greater than 15/h during REM sleep was a significant independent predictor of metabolic syndrome (adjusted OR, 7.08; 95% CI, 1.60–31.41; p = 0.010) after adjusting for age, body mass index, and non-REM AHI ≥ 15/h. In partial correlation analysis, REM AHI was significantly associated with the presence of metabolic syndrome after adjusting for age and BMI (r = 0.229, p = 0.042). Korean patients with OSA frequently had comorbid metabolic syndrome. Moderate to severe OSA during REM sleep may be a predictor of metabolic syndrome.

Purpose Muscle relaxation following electrical automatic massage (EAM) has been found to reduce fatigue, depression, stress, anxiety, and pain in individuals with various conditions. However, the effects of EAM have not been extensively explored in patients with Alzheimer's disease (AD). Materials and methods Here, we conducted a randomized controlled study to evaluate the effects of EAM on the cognitive and non-cognitive functions of patients with AD spectrum disorders. Results We found that EAM attenuated changes in attention-associated cognitive scores and subjective sleep quality relative to those in controls. Conclusion While further studies in a clinical setting are needed to support our findings, these encouraging results suggest that EAM may be an alternative therapy for the management of associated symptoms in AD (ClinicalTrials.gov ID: NCT03507192, 24/04/2018).

Background Approximately 10% to 30% of Alzheimer disease (AD) patients progress rapidly in severity and become more dependent on caregivers. Although several studies have investigated whether imaging biomarkers such as medial temporal atrophy (MTA) and posterior atrophy (PA) are useful for predicting the rapid progression of AD, their results have been inconsistent. Objective The study aims to investigate the association of visually rated MTA and PA with rapid disease progression in AD. Methods This was a retrospective cohort study of 159 AD patients who were initially diagnosed with mild AD and were followed for 1 year to determine whether they progressed rapidly (a decrease of three points or more on the Mini-Mental State Examination over 1 year). We used 5-point and 4-point visual rating scales to assess MTA and PA, respectively. MTA and PA scores for each patient were dichotomized as normal (without atrophy) or abnormal (atrophy). We performed a logistic regression analysis to determine the odds ratios (ORs) of MTA and PA for rapid disease progression with adjustment for covariates. Results Within the study population, 47 (29.6%) patients progressed rapidly. Visual assessment of the magnetic resonance imaging (MRI) scans revealed that 112 patients (70.4%) showed MTA, whereas 80 patients (50.3%) showed PA. The ORs with 95% confidence intervals for MTA and PA were 1.825 (0.819-4.070) and 2.844 (1.378-5.835), respectively. The association of visually assessed PA, but not MTA, with rapid progression was significant after adjustment for covariates. Conclusion In patients with mild AD, visual assessment of PA exhibits independent predictive value for rapid disease progression.

Background In patients with amyloid-positive mild cognitive impairment (MCI), neurodegenerative biomarkers such as medial temporal lobe atrophy (MTA) are useful to predict disease progression to dementia. Although posterior atrophy (PA) is a well-known neurodegenerative biomarker of Alzheimer’s disease, little is known about PA as a predictor in patients with amyloid-positive MCI. Methods We included 258 patients with amyloid-positive MCI with at least one follow-up visit, and who had low cerebrospinal fluid (CSF) β-amyloid1–42 concentration. Data were obtained from the Alzheimer’s Disease Neuroimaging Initiative study. We assessed PA and MTA on magnetic resonance imaging (MRI) using visual rating scales and retrospectively determined progression to dementia during the follow-up period of up to 3 years (median 24 months). The Cox proportional hazards model was used to analyze hazard ratios (HRs) of PA and MTA for disease progression. Additionally, subjects were divided into four groups according to brain atrophy pattern (no atrophy, MTA only, PA only, both MTA and PA), and HRs for disease progression were compared with the no atrophy reference group. Analyses were conducted with and without adjustment for CSF phosphorylated tau181p (p-tau) and baseline demographics. Results A total of 123 patients (47.7%) showed MTA and 174 patients (67.4%) showed PA. Of the total cohort, 139 cases (53.9%) progressed to dementia. PA and MTA were associated with an increased risk for progression to dementia (HR 2.244, 95% confidence interval (CI) 1.497–3.364, and HR 1.682, 95% CI 1.203–2.352, respectively). In the analysis according to atrophy pattern, HR (95% CI) for progression was 2.998 (1.443–6.227) in the MTA only group, 3.126 (1.666–5.864) in the PA only group, and 3.814 (2.045–7.110) in both MTA and PA group. These results remained significant after adjustment. Conclusions In patients with amyloid-positive MCI, PA could predict progression to dementia independently of MTA. Electronic supplementary material The online version of this article (doi:10.1186/s13195-017-0326-y) contains supplementary material, which is available to authorized users.

Inter- and intra-rater reliability. (DOCX 16 kb)

Comparison of volumetric measures of temporal and parietal regions according to disease progression to dementia. (DOCX 19 kb)

Visual rating of medial temporal lobe atrophy. (DOCX 14 kb)

문 형태로 신생아를 포함한 어떤 연령대에서도 발생할 수 있으 며, 전체 뇌졸중의 0.5-1%를 차지한다. 최근 급성 혹은 아급성 두통과 새로 발생한 발작(seizure) 환자에서의 자기공명영상 등 영상 진단 장치의 사용이 늘어나면서, 뇌정맥혈전증으로 진단되 는 환자 수가 늘어나고 있다. 뇌정맥혈전증의 위험인자는 크게 유전적 위험인자와 후천적 위험인자로 분류되며, 전자는 C단백 질결핍(protein C deficiency), S단백질결핍(protein S deficiency) 을 포함한 혈전유발성 경향, 결체조직질환 등이 있고, 후자는 수 술, 감염, 외상, 임신, 산욕기, 암, 외인성 호르몬, 약물, 항인지질 항체증후군(antiphospholipid antibody syndrome) 등이 있다. 저자들은 다른 유발 요인 없이 finasteride 복용에 의해 유발 된 뇌정맥혈전증 환자를 경험하여 보고하고자 한다.

Background Although medial temporal atrophy (MTA) is a useful imaging marker of the progression to dementia in mild cognitive impairment (MCI), substantial numbers of MCI patients without MTA still progress to dementia. Objective We investigated whether visual ratings of posterior atrophy (PA) on magnetic resonance imaging show independent predictive value for the progression to dementia in MCI patients. Methods This was a retrospective cohort study of elderly patients who visited Seoul National University Bundang Hospital between 2004 and 2012. A total of 148 patients who were initially diagnosed with MCI were followed for up to 3 years (median 22 months) to determine whether they progressed to dementia. We used 4-point and 5-point visual rating scales to assess PA and MTA, respectively. PA and MTA scores were dichotomized into normal (no atrophy) or abnormal (atrophy) in each patient. We performed a Cox regression analysis to examine the hazard ratios (HRs) of PA and MTA for the progression to dementia with adjustment for age, APOEɛ4 allele status, and baseline Mini-Mental State Examination score. Results Among the study population, 47 patients progressed to dementia. Visual assessment of the MRI scans revealed that 67 patients (45.3%) showed PA, whereas 85 patients (57.3%) showed MTA. The HRs with 95% confidence intervals for PA and MTA were 2.516 (1.244-5.091) and 4.238 (1.680-10.687), respectively. The predictive values of visually assessed PA and MTA remained significant, independent of the covariates. Conclusion Visual assessment of PA has independent predictive value for progression to dementia in MCI patients.

Transient monocular blindness (TMB) is a well-known warning symptom of impending cerebral or retinal infarction, which suggests vulnerable ipsilateral carotid disease. Instability of free-floating thrombus may cause recurrent artery-to-artery embolism. A recent study showed that a combination of clopidogrel and aspirin might reduce microthromboembolisms. Here, we report a patient with frequent TMB despite aspirin monotherapy whose symptom disappeared after the addition of clopidogrel. This is the first report of aspirin-resistant frequent TMB caused by thromboembolism from vulnerable plaque that remitted after the addition of clopidogrel. These findings highlight the need for a randomized controlled trial to illustrate the most efficacious treatment strategy in this situation.