Descending Colon Perforation Due to Ingestion of Foreign Body.

Foreign body ingestion is a common reason for emergency department (ED) visits, with rare complications necessitating immediate surgical intervention. This case report discusses diagnosis and treatment, emphasizing the importance of prompt intervention. A 45-year-old male with dentures presented with acute left abdominal pain. Diagnostic tests identified a foreign body in the descending colon, leading to laparoscopic surgery. Early laparoscopy offers a safe and reliable alternative to exploratory laparotomy. This case underscores the significance of swift diagnosis, preventing severe complications like peritonitis, obstruction, and hemorrhage. In conclusion, while foreign body ingestion is common, intestinal perforation remains extremely rare. Physicians should consider it in their differential diagnosis, with computed tomography (CT) and rapid surgical intervention as crucial components of proper management.

Appendicitis Caused by a Giant Appendicolith.

The coproliths of the appendix are accumulations of fecal remnants within its lumen. They are categorized based on their size into coproliths < 1cm, which are the most common, and giant coproliths, with a diameter > 2cm. It's important to note that the pathophysiology of acute appendicitis is characterized by the obstruction of the appendix lumen. This leads to distension due to the inability to expel secretions, ischemia, and ultimately rupture of its wall. This presentation discusses an interesting case of acute appendicitis caused by a giant coprolith. It also covers the clinical approach and information according to international literature. A 38-year-old man presented with sudden-onset right lower quadrant pain. Clinical examination revealed tenderness, a positive McBurney's point, elevated inflammation markers, and a radiopaque finding on an X-ray. A CT scan revealed a 2.5cm coprolith in the appendix. An exploratory laparoscopy revealed appendix wall rupture, followed by subumbilical incision appendicectomy and cleansing of purulent collection. The patient was discharged from the hospital on the fourth postoperative day without any complications, demonstrating a smooth recovery process. The presence of a coprolith predisposes the development of acute appendicitis. This condition is associated with a worse prognosis, as it increases the likelihood of perforation and the formation of intraperitoneal abscesses. This case underscores the clinical significance of giant coproliths as a potential etiology for acute appendicitis. Early recognition and timely surgical intervention are pivotal in achieving favorable patient outcomes.

Myelination and excitation-inhibition balance synergistically shape structure-function coupling across the human cortex.

Recent work has demonstrated that the relationship between structural and functional connectivity varies regionally across the human brain, with reduced coupling emerging along the sensory-association cortical hierarchy. The biological underpinnings driving this expression, however, remain largely unknown. Here, we postulate that intracortical myelination and excitation-inhibition (EI) balance mediate the heterogeneous expression of structure-function coupling (SFC) and its temporal variance across the cortical hierarchy. We employ atlas- and voxel-based connectivity approaches to analyze neuroimaging data acquired from two groups of healthy participants. Our findings are consistent across six complementary processing pipelines: 1) SFC and its temporal variance respectively decrease and increase across the unimodal-transmodal and granular-agranular gradients; 2) increased myelination and lower EI-ratio are associated with more rigid SFC and restricted moment-to-moment SFC fluctuations; 3) a gradual shift from EI-ratio to myelination as the principal predictor of SFC occurs when traversing from granular to agranular cortical regions. Collectively, our work delivers a framework to conceptualize structure-function relationships in the human brain, paving the way for an improved understanding of how demyelination and/or EI-imbalances induce reorganization in brain disorders.

Individual differences in T1w/T2w ratio development during childhood.

Myelination is a key developmental process that promotes rapid and efficient information transfer. Myelin also stabilizes existing brain networks and thus may constrain neuroplasticity, defined here as the brain's potential to change in response to experiences rather than the canonical definition as the process of change. Characterizing individual differences in neuroplasticity may shed light on mechanisms by which early experiences shape learning, brain and body development, and response to interventions. The T1-weighted/T2-weighted (T1w/T2w) MRI signal ratio is a proxy measure of cortical microstructure and thus neuroplasticity. Here, in pre-registered analyses, we investigated individual differences in T1w/T2w ratios in children (ages 4-10, n = 157). T1w/T2w ratios were positively associated with age within early-developing sensorimotor and attention regions. We also tested whether socioeconomic status, cognition (crystallized knowledge or fluid reasoning), and biological age (as measured with molar eruption) were related to T1w/T2w signal but found no significant effects. Associations among T1w/T2w ratios, early experiences, and cognition may emerge later in adolescence and may not be strong enough to detect in moderate sample sizes.

Individual differences in frontoparietal plasticity in humans.

Neuroplasticity, defined as the brain's potential to change in response to its environment, has been extensively studied at the cellular and molecular levels. Work in animal models suggests that stimulation to the ventral tegmental area (VTA) enhances plasticity, and that myelination constrains plasticity. Little is known, however, about whether proxy measures of these properties in the human brain are associated with learning. Here, we investigated the plasticity of the frontoparietal system by asking whether VTA resting-state functional connectivity and myelin map values (T1w/T2w ratios) predicted learning after short-term training on the adaptive n-back (n = 46, ages 18-25). We found that stronger baseline connectivity between VTA and lateral prefrontal cortex predicted greater improvements in accuracy. Lower myelin map values predicted improvements in response times, but not accuracy. Our findings suggest that proxy markers of neural plasticity can predict learning in humans.

The expanding horizons of network neuroscience: From description to prediction and control.

The field of network neuroscience has emerged as a natural framework for the study of the brain and has been increasingly applied across divergent problems in neuroscience. From a disciplinary perspective, network neuroscience originally emerged as a formal integration of graph theory (from mathematics) and neuroscience (from biology). This early integration afforded marked utility in describing the interconnected nature of neural units, both structurally and functionally, and underscored the relevance of that interconnection for cognition and behavior. But since its inception, the field has not remained static in its methodological composition. Instead, it has grown to use increasingly advanced graph-theoretic tools and to bring in several other disciplinary perspectives-including machine learning and systems engineering-that have proven complementary. In doing so, the problem space amenable to the discipline has expanded markedly. In this review, we discuss three distinct flavors of investigation in state-of-the-art network neuroscience: (i) descriptive network neuroscience, (ii) predictive network neuroscience, and (iii) a perturbative network neuroscience that draws on recent advances in network control theory. In considering each area, we provide a brief summary of the approaches, discuss the nature of the insights obtained, and highlight future directions.

Network controllability mediates the relationship between rigid structure and flexible dynamics.

Precisely how the anatomical structure of the brain supports a wide range of complex functions remains a question of marked importance in both basic and clinical neuroscience. Progress has been hampered by the lack of theoretical frameworks explaining how a structural network of relatively rigid interareal connections can produce a diverse repertoire of functional neural dynamics. Here, we address this gap by positing that the brain's structural network architecture determines the set of accessible functional connectivity patterns according to predictions of network control theory. In a large developmental cohort of 823 youths aged 8 to 23 years, we found that the flexibility of a brain region's functional connectivity was positively correlated with the proportion of its structural links extending to different cognitive systems. Notably, this relationship was mediated by nodes' boundary controllability, suggesting that a region's strategic location on the boundaries of modules may underpin the capacity to integrate information across different cognitive processes. Broadly, our study provides a mechanistic framework that illustrates how temporal flexibility observed in functional networks may be mediated by the controllability of the underlying structural connectivity.

[Ischemic stroke in coronavirus disease 2019]. / Ischämische Hirninfarkte bei Coronavirus-19-Erkrankung.

This article reports two cases of patients with coronavirus disease 2019 (COVID-19) in which occlusion of large cerebral arteries occurred. These occurred in a female patient in the early stage of COVID-19 and in the second case in the late stage. One female patient could be successfully treated with i.v. thrombolysis and mechanical thrombectomy. Coagulopathy in the course of COVID-19 can result in severe stroke with poor outcome even in younger patients. With respect to the etiology of arterial occlusions (COVID-19-induced hypercoagulopathy, cardiomyopathy, vasculitis) there is a necessity for further research.

QSIPrep: an integrative platform for preprocessing and reconstructing diffusion MRI data.

Diffusion-weighted magnetic resonance imaging (dMRI) is the primary method for noninvasively studying the organization of white matter in the human brain. Here we introduce QSIPrep, an integrative software platform for the processing of diffusion images that is compatible with nearly all dMRI sampling schemes. Drawing on a diverse set of software suites to capitalize on their complementary strengths, QSIPrep facilitates the implementation of best practices for processing of diffusion images.

Decreased Basal Ganglia Volume in Cerebral Amyloid Angiopathy.

BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy (CAA) is a common pathology of the leptomeningeal and cortical small vessels associated with hemorrhagic and non-hemorrhagic brain injury. Given previous evidence for CAA-related loss of cortical thickness and white matter volume, we hypothesized that CAA might also cause tissue loss in the basal ganglia. METHODS: We compared basal ganglia volumes expressed as a percentage of total intracranial volume (pBGV) of non-demented patients with sporadic and hereditary CAA to age-matched healthy control (HC) and Alzheimer's disease (AD) cohorts. RESULTS: Patients with sporadic CAA had lower pBGV (n=80, 1.16%±0.14%) compared to HC (n=80, 1.30%±0.13%, P<0.0001) and AD patients (n=80, 1.23%±0.11%, P=0.001). Similarly, patients with hereditary CAA demonstrated lower pBGV (n=25, 1.26%±0.17%) compared to their matched HC (n=25, 1.36%±0.15%, P=0.036). Using a measurement of normalized basal ganglia width developed for analysis of clinical-grade magnetic resonance images, we found smaller basal ganglia width in patients with CAA-related lobar intracerebral hemorrhage (ICH; n=93, 12.35±1.47) compared to age-matched patients with hypertension-related deep ICH (n=93, 13.46±1.51, P<0.0001) or HC (n=93, 15.45±1.22, P<0.0001). Within the sporadic CAA research cohort, decreased basal ganglia volume was independently correlated with greater cortical gray matter atrophy (r=0.45, P<0.0001), increased basal ganglia fractional anisotropy (r=-0.36, P=0.001), and worse performance on language processing (r=0.35, P=0.003), but not with cognitive tests of executive function or processing speed. CONCLUSIONS: These findings suggest an independent effect of CAA on basal ganglia tissue loss, indicating a novel mechanism for CAA-related brain injury and neurologic dysfunction.

Lacunes, Microinfarcts, and Vascular Dysfunction in Cerebral Amyloid Angiopathy.

OBJECTIVE: To analyze the relationship of lacunes with cortical cerebral microinfarcts (CMIs), to assess their association with vascular dysfunction, and to evaluate their effect on the risk of incident intracerebral hemorrhage (ICH) in cerebral amyloid angiopathy (CAA). METHODS: The count and topography of lacunes (deep/lobar), CMIs, and white matter hyperintensity (WMH) volume were retrospectively analyzed in a prospectively enrolled CAA cohort that underwent high-resolution research MRIs. The relationship of lacunes with CMIs and other CAA-related markers including time to peak (TTP) of blood oxygen level-dependent signal, an established measure of vascular dysfunction, was evaluated in multivariate models. Adjusted Cox regression models were used to investigate the relationship between lacunes and incident ICH. RESULTS: The cohort consisted of 122 patients with probable CAA without dementia (mean age, 69.4 ± 7.6 years). Lacunes were present in 31 patients (25.4%); all but one were located in lobar regions. Cortical CMIs were more common in patients with lacunes compared to patients without lacunes (51.6% vs 20.9%, p = 0.002). TTP was not associated with either lacunes or CMIs (both p > 0.2) but longer TTP response independently correlated with higher WMH volume (p = 0.001). Lacunes were associated with increased ICH risk in univariate and multivariate Cox regression models (p = 0.048 and p = 0.026, respectively). CONCLUSIONS: Our findings show a high prevalence of lobar lacunes, frequently coexisting with CMIs in CAA, suggesting that these 2 lesion types may be part of a common spectrum of CAA-related infarcts. Lacunes were not related to vascular dysfunction but predicted incident ICH, favoring severe focal vessel involvement rather than global ischemia as their mechanism.

Off-label intravenous thrombolysis for early recurrent brain embolism associated with aortic arch thrombus.

Safety data of intravenous thrombolysis (IVT) in presence of aortic arch thrombus is scant. Furthermore, IVT is debatable in patients with prior recent stroke. We present a 51-year-old woman with recurrent major infarction 5 days after a minor left MCA territory stroke. She had a floating aortic arch thrombus and she was treated safely and effectively with off-label IVT. Patients with small infarct volumes and mild/no residual neurological deficits after an initial stroke might be considered for IVT in case of early recurrence. IVT may be reasonable in a context of acute severely disabling stroke associated with aortic arch thrombus.

White Matter Hyperintensity Burden Is Associated With Hippocampal Subfield Volume in Stroke.

White matter hyperintensities of presumed vascular origin (WMH) are a prevalent form of cerebral small-vessel disease and an important risk factor for post-stroke cognitive dysfunction. Despite this prevalence, it is not well understood how WMH contributes to post-stroke cognitive dysfunction. Preliminary findings suggest that increasing WMH volume is associated with total hippocampal volume in chronic stroke patients. The hippocampus, however, is a complex structure with distinct subfields that have varying roles in the function of the hippocampal circuitry and unique anatomical projections to different brain regions. For these reasons, an investigation into the relationship between WMH and hippocampal subfield volume may further delineate how WMH predispose to post-stroke cognitive dysfunction. In a prospective study of acute ischemic stroke patients with moderate/severe WMH burden, we assessed the relationship between quantitative WMH burden and hippocampal subfield volumes. Patients underwent a 3T MRI brain within 2-5 days of stroke onset. Total WMH volume was calculated in a semi-automated manner. Mean cortical thickness and hippocampal volumes were measured in the contralesional hemisphere. Total and subfield hippocampal volumes were measured using an automated, high-resolution, ex vivo computational atlas. Linear regression analyses were performed for predictors of total and subfield hippocampal volumes. Forty patients with acute ischemic stroke and moderate/severe white matter hyperintensity burden were included in this analysis. Median WMH volume was 9.0 cm3. Adjusting for intracranial volume and stroke laterality, age (ß = -3.7, P < 0.001), hypertension (ß = -44.7, P = 0.04), WMH volume (ß = -0.89, P = 0.049), and mean cortical thickness (ß = 286.2, P = 0.006) were associated with total hippocampal volume. In multivariable analysis, age (ß = -3.3, P < 0.001) and cortical thickness (ß = 205.2, P = 0.028) remained independently associated with total hippocampal volume. In linear regression for predictors of hippocampal subfield volume, increasing WMH volume was associated with decreased hippocampal-amygdala transition area volume (ß = -0.04, P = 0.001). These finding suggest that in ischemic stroke patients, increased WMH burden is associated with selective hippocampal subfield degeneration in the hippocampal-amygdala transition area.

White matter atrophy in cerebral amyloid angiopathy.

OBJECTIVE: We postulated that cerebral amyloid angiopathy (CAA) is associated with white matter atrophy (WMA) and that WMA can be related to cognitive changes in CAA. METHODS: White matter volume expressed as percent of intracranial volume (pWMV) of prospectively enrolled patients without dementia diagnosed with probable CAA was compared to age-matched healthy controls (HC) and patients with Alzheimer disease (AD). Cognitive scores were also sought to understand the potential effects of WMA on cognitive function. RESULTS: Patients with CAA (n = 72) had significantly lower pWMV (27.97% ± 2.63) when compared to age-matched HC (n = 72; mean difference [MD], 2.38%; p < 0.0001) and patients with AD (n = 72; MD, 1.57%; p < 0.0001). Differences were most pronounced in the posterior occipital regions in both comparisons. When comparisons were restricted to groups of patients with CAA but no intracerebral hemorrhage (n = 32) or hypertension (n = 32), and age-matched HC and AD, the significant differences were unaltered. Within the CAA cohort, higher age, lobar microbleed counts, and presence of hypertension were associated with lower pWMV (p = 0.0007, p = 0.031, and p = 0.003, respectively). All associations remained independent in multivariable analyses. Within the CAA cohort, higher pWMV independently correlated with better scores of executive function. CONCLUSIONS: Patients with CAA show WMA when compared to age-matched HC and patients with AD. WMA independently correlates with the number of lobar microbleeds, a marker of CAA severity. Consistent spatial patterns of WMA especially in posterior regions might be related to CAA. The association between WMA and measures of executive function suggests that WMA might represent an important mediator of CAA-related neurologic dysfunction.

Cortical superficial siderosis progression in cerebral amyloid angiopathy: Prospective MRI study.

OBJECTIVE: To investigate the prevalence, predictors, and clinical relevance of cortical superficial siderosis (cSS) progression in cerebral amyloid angiopathy (CAA). METHODS: Consecutive patients with symptomatic CAA meeting Boston criteria in a prospective cohort underwent baseline and follow-up MRI within 1 year. cSS progression was evaluated on an ordinal scale and categorized into mild (score 1-2 = cSS extension within an already present cSS focus or appearance of 1 new cSS focus) and severe progression (score 3-4 = appearance of ≥2 new cSS foci). Binominal and ordinal multivariable logistic regression were used to determine cSS progression predictors. We investigated future lobar intracerebral hemorrhage (ICH) risk in survival analysis models. RESULTS: We included 79 patients with CAA (mean age, 69.2 years), 56 (71%) with lobar ICH at baseline. cSS progression was detected in 23 (29%) patients: 15 (19%) patients had mild and 8 (10%) severe progression. In binominal multivariable logistic regression, ICH presence (odds ratio [OR], 7.54; 95% confidence interval [CI], 1.75-53.52; p = 0.016) and baseline cSS (OR, 10.41; 95% CI, 2.84-52.83; p = 0.001) were independent predictors of cSS progression. In similar models, presence of disseminated (but not focal) cSS at baseline (OR, 5.58; 95% CI, 1.81-19.41; p = 0.004) was an independent predictor of cSS progression. Results were similar in ordinal multivariable logistic regression models. In multivariable Cox regression analysis, severe cSS progression was independently associated with increased future ICH risk (HR, 5.90; 95% CI, 1.30-26.68; p = 0.021). CONCLUSIONS: cSS evolution on MRI is common in patients with symptomatic CAA and might be a potential biomarker for assessing disease severity and future ICH risk. External validation of these findings is warranted.

Spatial Signature of White Matter Hyperintensities in Stroke Patients.

Purpose: White matter hyperintensity (WMH) is a common phenotype across a variety of neurological diseases, particularly prevalent in stroke patients; however, vascular territory dependent variation in WMH burden has not yet been identified. Here, we sought to investigate the spatial specificity of WMH burden in patients with acute ischemic stroke (AIS). Materials and Methods: We created a novel age-appropriate high-resolution brain template and anatomically delineated the cerebral vascular territories. We used WMH masks derived from the clinical T2 Fluid Attenuated Inverse Recovery (FLAIR) MRI scans and spatial normalization of the template to discriminate between WMH volume within each subject's anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA) territories. Linear regression modeling including age, sex, common vascular risk factors, and TOAST stroke subtypes was used to assess for spatial specificity of WMH volume (WMHv) in a cohort of 882 AIS patients. Results: Mean age of this cohort was 65.23 ± 14.79 years, 61.7% were male, 63.6% were hypertensive, 35.8% never smoked. Mean WMHv was 11.58c ± 13.49 cc. There were significant differences in territory-specific, relative to global, WMH burden. In contrast to PCA territory, age (0.018 ± 0.002, p < 0.001) and small-vessel stroke subtype (0.212 ± 0.098, p < 0.001) were associated with relative increase of WMH burden within the anterior (ACA and MCA) territories, whereas male sex (-0.275 ± 0.067, p < 0.001) was associated with a relative decrease in WMHv. Conclusions: Our data establish the spatial specificity of WMH distribution in relation to vascular territory and risk factor exposure in AIS patients and offer new insights into the underlying pathology.

Microangiopathy underlying mixed-location intracerebral hemorrhages/microbleeds: A PiB-PET study.

OBJECTIVE: To test the hypothesis that patients with concomitant lobar and deep intracerebral hemorrhages/microbleeds (mixed ICH) have predominantly hypertensive small vessel disease (HTN-SVD) rather than cerebral amyloid angiopathy (CAA), using in vivo amyloid imaging. METHODS: Eighty Asian patients with primary ICH without dementia were included in this cross-sectional study. All patients underwent brain MRI and 11C-Pittsburgh compound B (PiB)-PET imaging. The mean cortical standardized uptake value ratio (SUVR) was calculated using cerebellum as reference. Forty-six patients (57.5%) had mixed ICH. Their demographic and clinical profile as well as amyloid deposition patterns were compared to those of 13 patients with CAA-ICH and 21 patients with strictly deep microbleeds and ICH (HTN-ICH). RESULTS: Patients with mixed ICH were younger (62.8 ± 11.7 vs 73.3 ± 11.9 years in CAA, p = 0.006) and showed a higher rate of hypertension than patients with CAA-ICH (p < 0.001). Patients with mixed ICH had lower PiB SUVR than patients with CAA (1.06 [1.01-1.13] vs 1.43 [1.06-1.58], p = 0.003). In a multivariable logistic regression model, mixed ICH was associated with hypertension (odds ratio 8.9, 95% confidence interval 1.4-58.4, p = 0.02) and lower PiB SUVR (odds ratio 0.03, 95% confidence interval 0.001-0.87, p = 0.04) compared to CAA after adjustment for age. Compared to HTN-ICH, mixed ICH showed a similar mean age (62.8 ± 11.7 vs 60.1 ± 14.5 years in HTN-ICH) and risk factor profile (all p > 0.1). Furthermore, PiB SUVR did not differ between mixed ICH (values presented above) and HTN-ICH (1.10 [1.00-1.16], p = 0.45). CONCLUSIONS: Patients with mixed ICH have much lower amyloid load than patients with CAA-ICH, while being similar to HTN-ICH. Overall, mixed ICH is probably caused by HTN-SVD, an important finding with clinical relevance.

Cerebral small vessel disease in patients with spontaneous cerebellar hemorrhage.

BACKGROUND: Spontaneous cerebellar-intracerebral hemorrhage (ICH) can be associated with both cerebral amyloid angiopathy (CAA) and hypertensive small vessel disease (HTN-SVD, i.e. arteriolosclerosis). To better understand the underlying microangiopathy of cerebellar-ICH, we aimed to evaluate the spatial distribution of supratentorial cerebral microbleeds (CMBs) and neuropathologic profiles in these patients. METHODS: We enrolled consecutive cerebellar-ICH patients. Clinical variables and MRI markers specific for CAA and HTN-SVD were assessed. Patients were classified into categories according to the topography (strictly-lobar, strictly-deep, and mixed) of supratentorial CMBs and comparisons were performed. Available neuropathological material was reviewed to evaluate the presence and severity of arteriolosclerosis and CAA. RESULTS: Ninety-eight cerebellar-ICH patients were enrolled. Fifty patients (51%) had at least one supratentorial CMB. Twelve patients (12%) had strictly lobar-CMBs, 12 patients (12%) showed strictly deep-CMBs and mixed-CMBs (lobar and deep CMBs) were present in 26 cerebellar-ICH patients (27%). In multivariable analysis, cerebellar-ICH patients with mixed-CMBs were associated with higher prevalence of hypertension (OR 4.9, 95% confidence interval [CI] 1.2-20, p = 0.017) but with lower prevalence of severe centrum-semiovale enlarged perivascular spaces (OR 0.2, CI 0.05-0.8, p = 0.024) when compared to cerebellar-ICH patients with strictly lobar-CMBs. Vascular risk factors and neuroimaging characteristics were similar between strictly deep-CMBs and mixed-CMBs. Six patients had available neuropathological material for analyses and they all showed some degree of arteriolosclerosis. CONCLUSIONS: Cerebellar-ICH patients frequently show supratentorial CMBs. The mixed-CMBs pattern appears to be the most common. Our radiological and pathological results suggest that the majority of cerebellar-ICH patients harbor HTN-SVD as dominant microangiopathy.

Cerebral Cortical Microinfarcts on Magnetic Resonance Imaging and Their Association With Cognition in Cerebral Amyloid Angiopathy.

Background and Purpose- We aimed to explore the association between presence of cerebral cortical microinfarcts (CMIs) on magnetic resonance imaging and other small-vessel disease neuroimaging biomarkers in cerebral amyloid angiopathy (CAA) and to analyze the role of CMIs on individual cognitive domains and dementia conversion. Methods- Participants were recruited from an ongoing longitudinal research cohort of eligible CAA patients between March 2006 and October 2016. A total of 102 cases were included in the analysis that assessed the relationship of cortical CMIs to CAA neuroimaging markers. Ninety-five subjects had neuropsychological tests conducted within 1 month of magnetic resonance imaging scanning. Seventy-five nondemented CAA patients had cognitive evaluation data available during follow-up. Results- Among 102 patients enrolled, 40 patients had CMIs (39%) on magnetic resonance imaging. CMIs were uniformly distributed throughout the cortex without regional predilection ( P=0.971). The presence of CMIs was associated with lower total brain volume (odds ratio, 0.85; 95% CI, 0.74-0.98; P=0.025) and presence of cortical superficial siderosis (odds ratio, 2.66; 95% CI, 1.10-6.39; P=0.029). In 95 subjects with neuropsychological tests, presence of CMIs was associated with impaired executive function (ß, -0.23; 95% CI, -0.44 to -0.02; P=0.036) and processing speed (ß, -0.24; 95% CI, -0.45 to -0.04; P=0.020). Patients with CMIs had a higher cumulative dementia incidence compared with patients without CMIs ( P=0.043), whereas only baseline total brain volume (hazard ratio, 0.76; 95% CI, 0.62-0.92; P=0.006) independently predicted dementia conversion. Conclusions- Magnetic resonance imaging-detected CMIs in CAA correlated with greater overall disease burden. The presence of CMIs was associated with worse cognitive performance, whereas only total brain atrophy independently predicted dementia conversion.