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Clinical and imaging characteristics of TIA and minor stroke patients with and without cognitive deficits at day 30
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Background
Temporary and permanent cognitive changes following transient ischemic attack/minor stroke have been described previously. It is unknown if persisting cognitive deficits in these patients are correlated with acute infarction identified using magnetic resonance imaging.
Aims
We tested the hypothesis that persistent cognitive impairment a...
Similar publications
Cerebral small vessel disease is a common disease in the older population and is recognized as a major risk factor for cognitive decline and stroke. Small vessel disease is considered a global brain disease impacting the integrity of neuronal networks resulting in disturbances of structural and functional connectivity. A core feature of cerebral sm...
Citations
... Furthermore, an increased risk of worsening of cognitive impairment has been associated with alterations in CVR parameters and hemodynamics [11]. Despite the potential interest of the connection between cognitive impairment and altered cerebrovascular hemodynamics, few studies examined such association in patients with acute cerebral ischemia [12][13][14]. Understanding this complex interplay is, however, critical for developing prevention, intervention, and rehabilitation strategies following acute cerebral ischemia. ...
The association between cerebral hemodynamics and cognitive impairment has been reported in neurodegenerative and cerebrovascular disorders (CVD). However, it is still unclear whether changes occur in the acute phase of CVD. Here we investigated cognitive and hemodynamic parameters and their association in patients with CVD during the acute and subacute phases. Seventy-three patients with mild stroke, not undergoing endovascular treatment, were recruited. All subjects were devoid of intracranial or external carotid stenosis, significant chronic cerebrovascular pathology, dementia or non-compensated cardiovascular diseases. Patients were evaluated within 7 days from symptoms onset (T1) and after 3 months (T2). Clinical and demographic data were collected. NIHSS, MoCA, FAB, and Word-Color Stroop test (WCST) were used to evaluate disease severity and cognitive functions. Basal hemodynamic parameters in the middle cerebral artery were measured with transcranial Doppler. Differences between T2 and T1, correlations between cognitive and hemodynamic variables at T1 and T2, as well as correlations between the T2-T1 variation in cognitive and hemodynamic parameters were assessed. At T1, cognitive performance of MoCA, FAB, and WCST was lower compared with T2; and pulsatility index, a parameter reflecting distal vascular resistance, was higher. However, no correlations between the changes in cognitive and hemodynamic variables were found; therefore, the two seems to be independent phenomena. In the acute phase, the linear association between cerebral blood flow and cognitive performances was lost, probably due to a differential effect of microenvironment changes and vascular-specific phenomena on cognition and cerebral hemodynamics. This relationship was partially restored in the subacute phase.
... We also found that pre-existing WMH and diabetes were predictive of PSCI development. Although the association between pre-existing WMH and PSCI development was expected, this was again replicated in our groups, a finding suggestive of the importance of pre-existing WMH on cognitive impairment after small subcortical infarctions [37][38][39]. Regarding diabetes, this finding is consistent with those of previous studies [40,41]. Diabetes represents a metabolically unhealthy condition and has been found to be associated with inflammation, which may aggravate the neuronal damage after stroke [42]. ...
Background
The effect of amyloid-β (Aβ) on cognitive impairment in patients with small subcortical infarction remains controversial, although a growing body of evidence shows a substantial overlap between Alzheimer’s disease (AD) and subcortical ischemic vascular dementia, another form of cerebral small vessel disease (cSVD). Therefore, we investigated the relationships between Aβ positivity and the development of post-stroke cognitive impairment (PSCI) in patients with small subcortical infarction.
Methods
We prospectively recruited 37 patients aged ≥ 50 years, with first-ever small subcortical infarction, who underwent amyloid positron emission tomography, 3 months after stroke at Korea University Guro Hospital. We also enrolled CU participants matched for age and sex with stroke patients for comparison of Aβ positivity. Patients were followed up at 3 and 12 months after the stroke to assess cognitive decline. Logistic and linear mixed-effect regression analyses were performed to identify the effect of Aβ positivity on PSCI development and long-term cognitive trajectories.
Results
At 3 months after stroke, 12/37 (32.4%) patients developed PSCI, and 11/37 (29.7%) patients had Aβ deposition. Aβ positivity (odds ratio [OR] = 72.2, p = 0.024) was predictive of PSCI development regardless of cSVD burden. Aβ positivity ( β = 0.846, p = 0.014) was also associated with poor cognitive trajectory, assessed by the Clinical Dementia Rating-Sum of Box, for 1 year after stroke.
Conclusions
Our findings highlight that Aβ positivity is an important predictor for PSCI development and cognitive decline over 1 year. Furthermore, our results provide evidence that anti-AD medications may be a strategy for preventing cognitive decline in patients with small subcortical infarctions.
... Recently, volumetric measures of WMH were employed to assess contributions to cognitive impairment sensitively and reliably, which added additional value to WMH grades. Crosssectional studies that have used WMH volume have suggested that a higher volume of WMH is associated with greater impairments in global cognition as well as perceptional speed, memory, processing speed, and executive function; however, these studies have showed a weak evidential effect (46)(47)(48). While some studies have investigated the effects of total WMH volume on cognition, the regional specificity of WMH volume has rarely been explored. ...
Background
White matter hyperintensity (WMH) is often described in acute lacunar stroke (ALS) patients. However, the specific relationship between regional WMH volume and persistent cognitive impairment remains unclear.
Methods
We enrolled patients with ALS who were hospitalized at the First Affiliated Hospital of Soochow University between January 2020 and November 2022. All patients were assessed for global cognitive function using the Montreal Cognitive Assessment (MoCA) scale at 14 ± 2 days and 6 months after the onset of ALS. Manifestations of chronic cerebral small vessel disease (CSVD) were assessed via MRI scan. The distributions of regional WMH were segmented, and their relationship with cognitive impairment was evaluated.
Results
A total of 129 patients were enrolled. Baseline frontal WMH volume (OR = 1.18, P = 0.04) was an independent risk factor for long-term cognitive impairment after ALS. Furthermore, the presence of WMH at the genu of the corpus callosum (GCC) at baseline (OR = 3.1, P = 0.033) was strongly associated with persistent cognitive decline. Multivariable logistic regression analysis showed that depression (OR = 6.252, P = 0.029), NIHSS score (OR = 1.24, P = 0.011), and albumin at admission (OR = 0.841, P = 0.032) were also important determinants of long-term cognitive impairment after ALS.
Conclusions
Our study found that WMH, especially frontal WMH volume and the presence of WMH at the GCC at baseline, independently contributed to long-term cognitive decline in ALS patients. This study provides new evidence of the clinical relationship between regional WMH volume and cognitive impairment in ALS patients.
... Another interesting issue is the combination of TIAs, minor strokes, and AIS in the same population. For instance, Sivakumar and colleagues [67] tested the hypothesis that persistent cognitive impairment after TIA/minor stroke can be predicted by the volume of diffusion-weighted imaging lesions. It is well-established that cognitive impairment is common after TIA/minor stroke. ...
Stroke survivors are at increased risk of developing depression and cognitive decline. Thus, it is crucial for both clinicians and stroke survivors to be provided with timely and accurate prognostication of post-stroke depression (PSD) and post-stroke dementia (PSDem). Several biomarkers regarding stroke patients’ propensity to develop PSD and PSDem have been implemented so far, leukoaraiosis (LA) being among them. The purpose of the present study was to review all available work published within the last decade dealing with pre-existing LA as a predictor of depression (PSD) and cognitive dysfunction (cognitive impairment or PSDem) in stroke patients. A literature search of two databases (MEDLINE and Scopus) was conducted to identify all relevant studies published between 1 January 2012 and 25 June 2022 that dealt with the clinical utility of preexisting LA as a prognostic indicator of PSD and PSDem/cognitive impairment. Only full-text articles published in the English language were included. Thirty-four articles were traced and are included in the present review. LA burden, serving as a surrogate marker of “brain frailty” among stroke patients, appears to be able to offer significant information about the possibility of developing PSD or cognitive dysfunction. Determining the extent of pre-existing white matter abnormalities can properly guide decision making in acute stroke settings, as a greater degree of such lesioning is usually coupled with neuropsychiatric aftermaths, such as PSD and PSDem.
... A meta-analysis including thirty-six prospective studies with 19,040 enrolled patients discovered that WMH at baseline was associated with a 14% increased risk of cognitive impairment, and periventricular WMH was related to a 1.51-fold risk of the occurrence of dementia [8]. Cross-sectional studies also suggested that WMHs with higher Fazekas visual grades were correlated with the impairment of specific cognitive domains, but some studies showed weak evidence of effects [9][10][11][12][13][14][15]. Schmidt et al. found that the WMH load was no longer obviously related to cognitive function when adding brain volume changes to the regression model [16]. ...
... Several studies have focused on the association between WMH and cognition, but controversies persist [11,12,[39][40][41]. Multiple population-based studies have determined that a larger volume of WMHs, accompanied by higher Fazekas visual grades, is associated with cognitive decline [8,13,15,17]. A meta-analysis reflected that WMHs were closely related to the incidence of cognitive impairment [17]. ...
... Secondly, focal lesions caused by WMHs can spread to remote areas through a number of pathophysiological changes [63]. In addition, studies found that WMHs and hippocampal atrophy had a cumulative effect, and periventricular WMHs were connected to hippocampal atrophy [15,17,35,44]. Taken together, the heterogeneity between WMH and cognition may be attributed to the white matter microstructural injury and remote WMH effects. ...
Background: The severity of white matter hyperintensity (WMH) in patients with acute lacunar stroke (ALS) may be not completely parallel to cognitive impairment. Controversies persist about the effects of WMH on cognitive dysfunction. It is vital to explore whether the association may be affected by certain factors and whether a subsequent subgroup analysis is necessary. The aim of this study was to evaluate the relationship between WMH and cognitive impairment in acute lacunar stroke patients and the possible causal factors. Methods: We continuously enrolled patients with ALS who were hospitalized at the First Affiliated Hospital of Soochow University between October 2017 and June 2022. The cognitive function of all patients was assessed by using the Montreal Cognitive Assessment (MoCA) scale 14 ± 2 days after the onset of AIS, and the results were adjusted to the education level. The MoCA scale was reevaluated at the 6-month (day 182 ± 7) follow-up by outpatient visit or video. Demographic and clinical data were collected. The manifestations of chronic cerebral small-vessel disease (CSVD), including the total Fazekas score and total CSVD burden score, were assessed with an MRI scan. A mismatch refers to an inconsistency between the severity of WMH and cognitive dysfunction. A Type 1 mismatch refers to cognitive impairment with mild WMH (total Fazekas score = 0–1), and a Type 2 mismatch refers to severe WMH (total Fazekas score = 5–6) in patients with normal cognitive function. Results: Among 213 enrolled ALS patients, 66 patients (31.0%) had cognitive dysfunction, and 40 patients (18.8%) had mismatches. Twenty-seven cases (12.7%) were Type 1 mismatched, and seventeen cases (8.0%) were Type 2 mismatched. Age, gender, fibrinogen and cerebral infarction history were independent risk factors for cognitive impairment in ALS patients. Imaging features, including moderate to severe WMH, deep WMH and the total CSVD burden score, were also independently associated with cognitive impairment. The patients in the mismatched group were older, had more severe deep WMH and had a higher occurrence of depression (p < 0.05). The NIHSS score, depression and microbleeds were significantly different between the Type 1 mismatched group and the matched group (p = 0.018, p = 0.012 and p = 0.047). Patients in the Type 2 mismatched group were male (p = 0.04), had a lower level of fibrinogen (p = 0.005), a lower incidence of CMBs (p = 0.003), a lower total CSVD burden score (p = 0.017), more severe paraventricular WMH (p = 0.035) and milder deep WMH (p = 0.026). Conclusions: Our study examined a homogeneous study cohort of recruited patients with symptomatic ALS. We found heterogeneity between WMH and cognitive function in ALS patients. Despite a similar WMH severity, some baseline clinical features and other conventional CSVD imaging characteristics may account for this heterogeneity phenomenon. Our findings provide data for the early diagnosis and prevention of cognitive impairment in ALS patients and suggest that the severity of WMH is not completely parallel to cognitive impairment. The white matter microstructural injury and remote WMH effects may account for the mismatch phenomenon. More attention should be paid to understanding the underlying mechanisms and finding new imaging markers.
... Other reports showed the association between cerebral hemodynamic alterations and cognitive performances in patients with acute cerebral ischemia. In the case of lacunar infarcts, the increase in PI has been correlated to impairment of executive functions (Sivakumar et al. 2017). The increase of PI measured proximally to the blood vessels reflects the increased distal vascular resistance and consequent reduction of diastolic flow that may depend on alterations of microcirculation secondary to subcortical ischemic events (Uzuner et al. 2013). ...
... Acute ischemic stroke The correlation between impairment of CVR and the occurrence of acute ischemic stroke in patients with severe internal carotid artery stenosis has been convincingly confirmed (Gur et al. 1996;Silvestrini et al. 1996;Silvestrini et al. 2000;Markus and Cullinane 2001;Cheng et al. 2012;Viticchi et al. 2021) Alterations of hemodynamic factors and CVR have been related to the final infarct volume, unfavorable long-term outcome and most neurologic complications after acute stroke (Alvarez et al. 2004) Cerebral hemodynamic parameters are progressively compromised according to stroke severity (Salinet et al. 2019) In lacunar infarcts, the increase in PI has been correlated with impairment of executive functions (Sivakumar et al. 2017) A recent pilot study and suggested that hemodynamic alterations may contribute at worsening cognitive performances transiently, during the first 3-6 months following acute subcortical ischemia (Suministrado et al. 2017) Cerebral hemodynamic impairment plays a significant pathophysiological role in the acute phase of cerebral ischemia, and somehow predicts stroke severity, progression and long-term outcome Content courtesy of Springer Nature, terms of use apply. Rights reserved. ...
The regulation of cerebral blood flow (CBF) is a complex and tightly controlled function ensuring delivery of oxygen and nutrients and removal of metabolic wastes from brain tissue. Cerebral vasoreactivity (CVR) refers to the ability of the nervous system to regulate CBF according to metabolic demands or changes in the microenvironment. This can be assessed through a variety of nuclear medicine and imaging techniques and protocols. Several studies have investigated the association of CVR with physiological and pathological conditions, with particular reference to the relationship with cognitive impairment and cerebrovascular disorders (CVD). A better understanding of the interaction between CVR and cognitive dysfunction in chronic and particularly acute CVD could help improving treatment and rehabilitation strategies in these patients. In this paper, we reviewed current knowledge on CVR alterations in the context of acute and chronic CVD and cognitive dysfunction. Alterations in CVR and hemodynamics have been described in patients with both neurodegenerative and vascular cognitive impairment, and the severity of these alterations seems to correlate with CVR derailment. Furthermore, an increased risk of cognitive impairment progression has been associated with alterations in CVR parameters and hemodynamics. Few studies have investigated these associations in acute cerebrovascular disorders and the results are inconsistent; thus, further research on this topic is encouraged.
... In a prospective cohort study of 115 patients with TIA/minor stroke (NIHSS ≤ 3) recruited within 72 h of onset in Alberta, Canada, with cognitive testing at baseline, 7-days, 30-days, and 90-days post-event, cognitive impairment rates (defined as MoCA score < 26) were similar in patients with (47/91, 52%) and without diffusion-weighted imaging lesions (13/24, 54). However, persisting impairment at 30days was correlated with WMH volumes, suggesting that subclinical cognitive impairment and/or impaired ability to compensate for the effects of acute ischemic infarcts may be at play [25]. Age is by far the most consistent risk factor for cognitive decline after TIA and the least surprising. ...
... In a prospective cohort study of 115 patients with TIA/minor stroke (NIHSS ≤ 3) recruited within 72 h of onset in Alberta, Canada, with cognitive testing at baseline, 7-days, 30-days, and 90-days post-event, cognitive impairment rates (defined as MoCA score < 26) were similar in patients with (47/91, 52%) and without diffusionweighted imaging lesions (13/24, 54). However, persisting impairment at 30-days was correlated with WMH volumes, suggesting that subclinical cognitive impairment and/or impaired ability to compensate for the effects of acute ischemic infarcts may be at play [25]. ...
There is now considerable evidence that Transient Ischemic Attack (TIA) carries important sequelae beyond the risk of recurrent stroke, particularly with respect to peri-event and post-event cognitive dysfunction and subsequent cognitive decline. The occurrence of a TIA could provide an important window in understanding the relationship of early mixed vascular-neurodegenerative cognitive decline, and by virtue of their clinical relevance as a “warning” event, TIAs could also furnish the opportunity to act preventatively not only for stroke prevention but also for dementia prevention. In this review, we discuss the current state of the literature regarding the cognitive sequelae associated with TIA, reviewing important challenges in the field. In particular, we discuss definitional and methodological challenges in the study of TIA-related cognitive impairment, confounding factors in the cognitive evaluation of these patients, and provide an overview of the evidence on both transient and long-term cognitive impairment after TIA. We compile recent insights from clinical studies regarding the predictors and mediators of cognitive decline in these patients and highlight important future directions for work in this area.
... Therefore, during cerebral ischemia or hypoperfusion, these areas are prone to ischemic changes and can result in changes to the imaging characteristics [4] (Markus et al., 2000). If the case is complicated by risk factors for cerebrovascular disease such as age [5] (Lin et al., 2017b), hypertension [6] Sivakumar et al., 2017), and depression. Importantly, many of these co-morbidities can lead to impaired memory function. ...
... Multiple population-based studies have determined the correlation between WMH volume and whole-brain cognitive decline. Cross-sectional studies suggest that a larger volume of WMHs, accompanied by higher Fazekas visual grades, associates with lower functioning of the entire brain or with specific regional cognitive performance deficits, but these studies show a weak evidential effect [7,21,22]. However, current research reveals that WMHs are particularly relevant to decreased information processing speed and executive function [23]. ...
White matter hyperintensities (WMHs) of presumed vascular origin are one of the imaging markers of cerebral small-vessel disease, which is prevalent in older individuals and closely associated with the occurrence and development of cognitive impairment. The heterogeneous nature of the imaging manifestations of WMHs creates difficulties for early detection and diagnosis of vascular cognitive impairment (VCI) associated with WMHs. Because the underlying pathological processes and biomarkers of WMHs and their development in cognitive impairment remain uncertain, progress in prevention and treatment is lagging. For this reason, this paper reviews the status of research on the features of WMHs related to VCI, as well as mediators associated with both WMHs and VCI, and summarizes potential treatment strategies for the prevention and intervention in WMHs associated with VCI.
... Single-factor binary logistic regression analysis of cognitive impairment group in severe stroke patients showed that the number of CMB, PVS, lacuna, WMH Fazekas score, and total CSVD scores all had a significant correlation (P < 0.05). Multivariate binary logistic regression analysis showed that the number of PVS, WMH Fazekas score, and total CSVD score were independent factors of cognitive impairment in severe brain, which was consistent with the results of the Sivakumar et al. [18], indicating that patients with severe stroke combined with the CSVD scores of the above items were relatively more likely to have cognitive impairment after stroke. After linear regression model analysis and correcting for risk factors, it was found that only the MOCA score, visual space and executive function, attention, and memory were significantly negatively correlated (P < 0.05), which was basically consistent with the research results of Liang et al. [19] on the correlation between total MRI cerebrovascular disease and cognitive impairment, indicating that it mainly affected attention, memory, and visual space and executive function. ...
The purpose of this paper is to explore the impact of magnetic resonance imaging (MRI) image features based on convolutional neural network (CNN) algorithm and conditional random field on the diagnosis and mental state of patients with severe stroke. 208 patients with severe stroke who all received MRI examination were recruited as the research objects. According to cerebral small vascular disease (CSVD) score, the patients were divided into CSVD 0∼4 groups. The patients who completed the three-month follow-up were classified into cognitive impairment group (124 cases) and the noncognitive impairment group (84 cases) according to the cut-off point of the Montreal cognitive assessment (MOCA) scale score of 26. A novel image segmentation algorithm was proposed based on U-shaped fully CNN (U-Net) and conditional random field, which was compared with the fully CNN (FCN) algorithm and U-Net algorithm, and was applied to the MRI segmentation training of patients with severe stroke. It was found that the average symmetric surface distance (ASSD) (3.13 ± 1.35), Hoffman distance (HD) (28.71 ± 9.05), Dice coefficient (0.78 ± 1.35), accuracy (0.74 ± 0.11), and sensitivity (0.85 ± 0.13) of the proposed algorithm were superior to those of FCN algorithm and U-Net algorithm. There were significant differences in the MOCA scores among the five groups of patients from CSVD 0 to CSVD 4 in the three time periods (0, 1, and 3 months) (P
