1,721,207 research outputs found
Domain-specific trends in cognitive impairment after acute ischaemic stroke
No full textLittle is known about the pattern of subacute
cognitive domain impairments after ischaemic stroke, nor
the temporal evolution of such impairments. Our objective
was to investigate the pattern of cognitive impairment in
different neuropsychological domains up to a year after
ischaemic stroke. We included prospectively collected data
from an observational database of stroke patients at the
National Hospital for Neurology and Neurosurgery, Queen
Square, London, UK. Patients were categorised into temporal
groups according to the time between the index
stroke and neuropsychological profiling. The prevalence of
impairment in different cognitive domains was then compared
between these categories. The final cohort consisted
of 209 patients. Frontal executive function, perceptual and
nominal skills all showed a strong trend, with levels of
impairment of approximately 30 % at\1 month and less
than half this at[3 months (p\0.05). Speed and attention
was the most impaired domain, but had the greatest trend
for decreasing impairment, from 72.4 % acutely to 37.9 %
after 3 months (p\0.01). By contrast, we found that
impairment in visual and verbal memory showed no statistically
significant change over time. Our results suggest a
domain-specific improvement in cognition after ischaemic
stroke. Early assessments may overestimate longer term
cognitive deficits, particularly in speed and attention and
perceptual functions. The domain-specific improvement
patterns may help to inform long-term rehabilitation plans,
which should not be based solely on cognitive assessments
undertaken within the first month after stroke
Cerebral microbleeds and vascular cognitive impairment
No full textVascular cognitive impairment (VCI) is a key healthcare challenge
facing all aging Western societies, second only to Alzheimer's Disease
(AD) as a cause of dementia [1]. Initial concepts of VCI invoked cortical
or subcortical infarction – leading to the terms “multi-infarct
dementia” and “post-stroke dementia”. However subcortical small
vessel disease (often not causing acute or overt clinical symptoms)
also plays a critical role in VCI [2–4]. MRI is the most important tool for
detecting and quantifying small vessel diseases, and forms part of
current diagnostic criteria for vascular dementia [1]. MRI manifestations
of small vessel diseases including white matter hyperintensities
(WMH: bright signal areas on T2-weighted or FLAIR images including
leukoaraiosis) and lacunes have been recognized for many years.
Cerebral microbleeds (CMBs) – small, perviascular haemorrhages
seen as well-demarcated, rounded lesions on MRI sequences sensitive
to magnetic susceptibility – are also now recognized as a manifestation
of small vessel pathology [5] (Fig. 1), but their clinical impact on
cognition remains uncertain [6]. This review will consider how CMBs
may be relevant in the study of VCI
Timing of anticoagulant after recent ischaemic stroke in patients with atrial fibrillation
No full textBackground About 13–26% of all acute ischaemic strokes are related to non-valvular atrial fibrillation, the most common cardiac arrhythmia globally. Deciding when to initiate oral anticoagulation in patients with non-valvular atrial fibrillation is a longstanding, common, and unresolved clinical challenge. Although the risk of early recurrent ischaemic stroke is high in this population, early oral anticoagulation is suspected to increase the risk of potentially harmful intracranial haemorrhage, including haemorrhagic transformation of the infarct. This assumption, and current treatment guidelines, are based on historical, mostly observational data from patients with ischaemic stroke and atrial fibrillation treated with heparins, heparinoids, or vitamin K antagonists (VKAs) to prevent recurrent ischaemic stroke. Randomised controlled trials have subsequently shown that direct oral anticoagulants (DOACs; ie, apixaban, dabigatran, edoxaban, and rivaroxaban) are at least as effective as VKAs in primary and secondary prevention of atrial fibrillation-related ischaemic stroke, with around half the risk of intracranial haemorrhage. However, none of these DOAC trials included patients who had experienced ischaemic stroke recently (within the first few weeks). Clinicians therefore remain uncertain regarding when to commence DOAC administration after acute ischaemic stroke in patients with atrial fibrillation.
Recent developments Prospective observational studies and two small randomised trials have investigated the risks and benefits of early DOAC-administration initiation (most with a median delay of 3–5 days) in mild-to-moderate atrial fibrillation-associated ischaemic stroke. These studies reported that early DOAC treatment was associated with a low frequency of clinically symptomatic intracranial haemorrhage or surrogate haemorrhagic lesions on MRI scans, whereas later DOAC-administration initiation (ie, >7 days or >14 days after index stroke) was associated with an increased frequency of recurrent ischaemic stroke.
Where next? Adequately powered randomised controlled trials comparing early to later oral anticoagulation with DOACs in ischaemic stroke associated with atrial fibrillation are justified to confirm the acceptable safety and efficacy of this strategy. Four such randomised controlled trials (collectively planned to include around 9000 participants) are underway, either using single cutoff timepoints for early versus late DOAC-administration initiation, or selecting DOAC-administration timing according to the severity and imaging features of the ischaemic stroke. The results of these trials should help to establish the optimal timing to initiate DOAC administration after recent ischaemic stroke and whether the timing should differ according to stroke severity. Results of these trials are expected from 2021.Background: About 13–26% of all acute ischaemic strokes are related to non-valvular atrial fibrillation, the most common cardiac arrhythmia globally. Deciding when to initiate oral anticoagulation in patients with non-valvular atrial fibrillation is a longstanding, common, and unresolved clinical challenge. Although the risk of early recurrent ischaemic stroke is high in this population, early oral anticoagulation is suspected to increase the risk of potentially harmful intracranial haemorrhage, including haemorrhagic transformation of the infarct. This assumption, and current treatment guidelines, are based on historical, mostly observational data from patients with ischaemic stroke and atrial fibrillation treated with heparins, heparinoids, or vitamin K antagonists (VKAs) to prevent recurrent ischaemic stroke. Randomised controlled trials have subsequently shown that direct oral anticoagulants (DOACs; ie, apixaban, dabigatran, edoxaban, and rivaroxaban) are at least as effective as V..
Underestimation of cognitive impairments by the Montreal Cognitive Assessment (MoCA) in an acute stroke unit population.
No full textBackground and purpose: The Montreal Cognitive Assessment (MoCA) is an increasingly popular clinical screening
tool for detecting cognitive impairment in stroke, but fewstudies have directly compared performance on the
MoCAwith neuropsychological assessment. Our retrospective study examined the extent towhich intact performance
on the MoCA reflects intact cognition as determined by neuropsychological assessment.
Methods: In this retrospective study, cognitive profiles for 136 acute stroke patients admitted to the Acute Stroke
Unit who had available MoCA and neuropsychological assessment data were examined.
Results: 22% of our patientswere deemed cognitively intact on theMoCA.Of these, 78%were found to be impaired
(≤5%ile) on neuropsychological assessment in one or more cognitive domains. The most common impairments
were in general intelligence, information processing speed and visual memory; three areas not assessed by the
MoCA. In addition, a high proportion (up to 59%) of patients who scored the maximum points in one of the
MoCA-specified domains were impaired on comparable neuropsychological assessment.
Conclusions: Our findings suggest that although theMoCA may be a useful screening tool post-stroke in detecting
gross impairments, neuropsychological assessment is still necessary for a comprehensive and reliable detection
of domain-specific cognitive deficits, which can more reliably inform us for realistic goal setting and vocational
advice vital for effective rehabilitation
Strictly lobar microbleeds are associated with executive impairment in patients with ischemic stroke or transient ischemic attack
No full textBACKGROUND AND PURPOSE-: Cerebral microbleeds (CMBs) are a marker of small vessel diseases, including hypertensive arteriopathy and cerebral amyloid angiopathy, and may be associated with cognitive impairment. The relationship between CMBs and cognitive function in ischemic cerebrovascular disease remains uncertain. We, therefore, investigated the cognitive impact of CMBs in a cohort of patients with ischemic stroke or transient ischemic attack. METHODS-: All patients underwent detailed and comprehensive neuropsychological testing and standardized MRI, including fluid attenuation inversion recovery, T1, T2, and gradient-recalled echo T2*-weighted sequences. CMBs, white matter changes, lacunes, and territorial cortical infarcts (defined by standardized criteria) were identified, and associations with cognition assessed. RESULTS-: Three hundred twenty patients with a diagnosis of ischemic stroke or transient ischemic attack were included. Of these, 72 (22.5%) had at least 1 CMB. Of all t..
MRI-visible perivascular spaces: Relationship to cognition and small vessel disease MRI markers in ischaemic stroke and TIA
Full text linkBackground MRI-visible perivascular spaces (PVS) are potential neuroimaging markers of cerebral small vessel disease, but their functional significance and mechanisms remain uncertain. We investigated the association between PVS and cognitive impairment, and other MRI markers of small vessel disease, in a patient cohort of ischaemic stroke/transient ischaemic attack (TIA) referrals. Methods Data were collected from a prospective observational database. Standardised detailed neuropsychological testing was performed. A validated visual rating scale on T2-weighted MRI was used to categorise PVS severity; validated scales were used to assess white matter hyperintensities (WMH), cerebral microbleeds (CMB) and lacunes. Results We included 246 patients (45.1% female, mean age 62 years). No significant association between PVS severity grade in any brain region and impairment in any cognitive domain was identified. In multivariable analysis, WMH and hypertension (but not age) were independently associated with basal ganglia PVS severity (OR: 1.27; p<0.0001 and OR: 4.89; p=0.013, respectively). Increasing PVS severity in the basal ganglia was associated with lacunar stroke subtype (p<0.0001). Age and hypertension (but not WMH or lacunar stroke subtype) were independently associated with centrum semiovale PVS severity (OR: 1.19; p=0.013 and OR: 3.71; p=0.007, respectively). Conclusions PVS do not have an independent association with cognitive impairment in patients with ischaemic stroke or TIA. The associations with clinicalradiological factors are consistent with the hypothesis that PVS reflect cerebral small vessel disease; the different associations for basal ganglia and centrum semiovale PVS might indicate different underlying small vessel arteriopathies according to PVS anatomical distribution, but this requires further study
Cognitive dysfunction and depression in Fabry disease: a systematic review.
No full textBackground Fabry disease, an X-linked lysosomal storage
disorder, leads to multi-organ dysfunction, including cerebrovascular
disease and psychological disorders. However, the
prevalence and pattern of associated cognitive dysfunction is
not well understood.
Objectives To investigate whether there is reliable evidence
for neuropsychological impairment in patients with Fabry
disease and which cognitive domains are affected. To estimate
the prevalence of and factors associated with depression in
patients with Fabry disease.
Method Qualitative systematic review of the literature of
studies conducting neuropsychological assessment or measuring
the prevalence of depression in adults with Fabry disease
using the preferred reporting items for systematic reviews and
meta-analysis (PRISMA) guidelines where appropriate.
Results There is some evidence for neuropsychological impairment
in Fabry disease in executive functioning, information
processing speed and attention, with preservation of:
general intellectual functioning, memory, naming, perceptual
functioning and global cognitive functioning. Prevalence rates
of depression in Fabry disease ranged from 15%to 62%,with
the largest study to date reporting a prevalence rate of 46 %.
The most common factor associated with depression was
neuropathic pain, both directly and indirectly by affecting
social and adaptive functioning.
Conclusion Our review suggests that Fabry disease may be
associated with a characteristic pattern of cognitive deficits and
a high prevalence of psychological disorders such as depression
but highlights the limited available data. Exploring the nature of
cognitive impairment in Fabry disease using standardised neuropsychological
assessment, brain imaging and measures of
depression is an important task for future research
Cerebral Microbleeds and Long-Term Cognitive Outcome: Longitudinal Cohort Study of Stroke Clinic Patients
No full textBackground: Vascular cognitive impairment causes significant disability in the elderly and is common following ischaemic stroke. Although the underlying mechanisms and prognostic factors remain unclear, small vessel diseases are known to contribute. Cerebral microbleeds (CMBs) are a magnetic resonance imaging (MRI) manifestation of small vessel diseases and may contribute to vascular cognitive impairment, particularly frontal-executive functions. We hypothesized that baseline CMBs would predict long-term cognitive outcome, specifically frontal-executive function. Methods: A cohort of consecutive patients found to have CMBs when first referred to a stroke clinic, together with a CMB-free control group matched for age, gender and clinicoradiological characteristics, were invited for follow-up cognitive assessment a median of 5.7 years later. MRI and detailed cognitive assessment (including current intellectual function, verbal memory, visual memory, naming skills, perceptual functions, frontal-executive functions; and speed and attention) were performed at baseline and follow-up. Patients were classified (blinded to MRI and clinical data) as impaired or unimpaired in each domain using predefined criteria. We compared the prevalence of cognitive impairments in each domain at baseline and follow-up and investigated clinical and radiological predictors [including baseline CMBs and white matter changes (WMCs)] of frontal-executive cognitive impairment. Results: Of the original cohort of 55 patients, 13 died without follow-up. Twenty-six of the surviving patients (9 with, 17 without baseline CMBs) agreed to follow-up neuropsychological assessment; 21 of these patients had a repeat MRI scan. The median number of cognitive domains impaired increased, regardless of the presence of baseline CMBs (with baseline CMBs: median 3, range 0–5 at follow-up vs. median 2, range 0–2 at baseline, p = 0.016; without CMBs: median 1.0, range 0–5 at follow-up vs. median 0, range 0–5 at baseline, p = 0.035). Frontal-executive impairment at follow-up was more prevalent in patients with baseline CMBs than in those without (78 vs. 29%, p = 0.038). The presence of baseline CMBs predicted frontal-executive impairment at follow-up (OR 8.40, 95% CI 1.27–55.39, p = 0.027). Fifty percent of patients with CMBs versus 8% of patients without baseline CMBs developed new CMBs (p = 0.047). The severity of WMCs increased; the difference was statistically significant only in patients without baseline CMBs (p = 0.027). There were no new cortical infarcts. Conclusion: In stroke clinic patients, CMBs are consistently associated with frontal-executive impairment; baseline CMBs are associated with frontal-executive impairment at follow-up after 5.7 years. The presence of CMBs has prognostic relevance for long-term cognitive outcome in stroke clinic patients, and may help to optimally target preventive strategies in individuals at highest risk of cognitive decline
Applied Clinical Neuroimaging in Cerebral Amyloid Angiopathy and Spontaneous Intracerebral Haemorrhage
Full text linkSporadic cerebral amyloid angiopathy is a common small vessel disease that preferentially involves small cortical and leptomeningeal arteries due to progressive amyloid-β deposition in their walls. Cerebral amyloid angiopathy occurs frequently in elderly people, and is a common and important cause of symptomatic lobar intracerebral haemorrhage and cognitive impairment. There is currently a growing interest in cerebral amyloid angiopathy, at least partly thanks neuroimaging, which now allows an unprecedented ability to investigate the disease dynamics in vivo using MRI to reveal complex patterns of cerebral bleeding and ischaemia. The detection of CAA during life is becoming an increasingly important challenge, since approaches of prevention or treatment (disease-modification) are now emerging as realistic possibilities. Determining the most promising treatments requires development of reliable biomarkers, the goal of my research. The main objective of this PhD thesis is to provide new insights into potential clinical and applied clinical neuroimaging biomarkers in patients with cerebral amyloid angiopathy. This is accomplished by a portfolio of research studies investigating: (a) the clinical and radiological spectrum of transient focal neurological episodes as a potential clinical clue for cerebral amyloid angiopathy; (b) cortical superficial siderosis, a distinct pattern on bleeding in the brain, as both a diagnostic and a prognostic marker of cerebral amyloid angiopathy; (c) MRI-visible perivascular spaces topography, as a new marker of small vessel disease and cerebral amyloid angiopathy; (d) potential pathological, neuroimaging and genetic differences in patients with pathology-proven CAA with and without intracerebral haemorrhage and presents evidence for different disease phenotypes; (e) the evidence whether the presence and burden of cerebral microbleeds on MRI scans is associated with an increased risk of recurrent spontaneous ICH, and if this risk is different according to MRI-defined microangiopathy subtype, in a meta-analysis
Cognitive dysfunction in patients with cerebral microbleeds on T2*-weighted gradient-echo MRI.
No full textGradient echo T2*-weighted MRI has high sensitivity in detecting cerebral microbleeds, which appear as small dot-like hypointense lesions. Microbleeds are strongly associated with intracerebral haemorrhage, hypertension, lacunar stroke and ischaemic small vessel disease, and have generated interest as a marker of bleeding-prone microangiopathy. Microbleeds have generally been considered to be clinically silent; however, since they are located in widespread cortical and basal ganglia regions and are histologically characterized by tissue damage, we hypothesized that they would cause cognitive dysfunction. We therefore studied patients with microbleeds (n = 25) and a non-microbleed control group (n = 30) matched for age, gender and intelligence quotient. To avoid the confounding effects of coexisting cerebrovascular disease, the groups were also matched for the extent of MRI-visible white matter changes of presumed ischaemic origin, location of cortical strokes, and for the proportion of patients with different stroke subtypes (including lacunar stroke). A battery of neuropsychological tests was used to assess current intellectual function, verbal and visual memory, naming and perceptual skills, speed and attention and executive function. Microbleeds were most common in the basal ganglia but were also found in frontal, parieto-occipital, temporal and infratentorial regions. There was a striking difference between the groups in the prevalence of executive dysfunction, which was present in 60% of microbleed patients compared with 30% of non-microbleed patients (P = 0.03). Logistic regression confirmed that microbleeds (but not white matter changes) were an independent predictor of executive impairment (adjusted odds ratio = 1.32, 95% confidence interval 1.01-1.70, P = 0.04). Patients with executive dysfunction had more microbleeds in the frontal region (mean count 1.54 versus 0.03; P = 0.002) and in the basal ganglia (mean 1.17 versus 0.32; P = 0.048). There was a modest correlation between the number of microbleeds and the number of cognitive domains impaired (r = 0.44, P = 0.03). This study provides novel evidence that microbleeds are associated with cognitive dysfunction, independent of the extent of white matter changes of presumed ischaemic origin, or the presence of ischaemic stroke. The striking effect of microbleeds on executive dysfunction is likely to result from associated tissue damage in the frontal lobes and basal ganglia. These findings have implications for the diagnosis of stroke patients with cognitive impairment, and for the appropriate use of antihypertensive and antiplatelet treatments in these patients
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