A decade after stroke, young stroke survivors continue to suffer from cognitive impairment. However, it is not known whether this long-term cognitive outcome is caused in part by further cognitive ...decline or solely by incomplete recovery from the acute effects of ischemic stroke. We studied changes in three cognitive domains over a 9-year follow-up period after first-ever and only ischemic stroke.
In this prospective, two-center cohort study, we recruited consecutive 18-65 year-old patients with acute stroke between 2007 and 2009, along with demographically matched stroke-free controls. We performed comprehensive neuropsychological assessments at 3 months, 2, and 9 years after stroke, and we also performed neurological examinations at the time of inclusion and at the 9-year follow-up. We assessed the associations among stroke, follow-up time and long-term cognitive outcomes using repeated-measures analysis of variance.
The subjects comprised 85 patients who had had their first-ever and only ischemic stroke (mean age 53 years at inclusion), along with 31 stroke-free demographic controls. We compared the cognitive changes in patients to those in controls over a 9-year follow-up. After initial recovery between 3 months and 2 years after stroke, patients showed a decline in memory between 2 and 9 years after stroke compared to controls within the same time interval (immediate recall
< 0.001; delayed recall
< 0.001; list learning
< 0.001). Other than memory, we found no difference in cognitive changes between poststroke patients and controls.
Our main finding was memory decline over a decade in young first-ever stroke patients with no further stroke or neurodegenerative disease. Our study extends the previous results of further memory decline in elderly stroke survivors to young stroke survivors.
Young stroke survivors might be at risk of memory decline over the decade following the stroke.
The Patlak plot analysis of dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) allows estimation of blood–brain barrier (BBB) leakage following temporary focal cerebral ischemia. Thus ...far, a systematic and quantitative in vivo evaluation of post-ischemic BBB leakage is lacking. Here, using DCE-MRI and the Patlak plot method, we quantitatively assessed BBB leakage in rats at the following time-points after reperfusion: 25 min, 2, 4, 6, 12, 18, 24, 36, 48, and 72 h, and 1, 2, 3, 4, and 5 weeks. Sham-operated animals served as controls. Data collected for each time-point were: the blood-to-brain transfer rate constant (
K
i) of the contrast agent gadolinium, distribution volume (
V
p), ischemic lesion volume, and apparent diffusion coefficient (ADC) values. Compared to controls,
K
i, measured at all time-points, except for 5 weeks, appeared significantly different (
p
<
0.001). At several time-points (25 min, 48 and 72 h, 4 and 5 weeks),
V
p was similar compared to that of controls, but for the remaining groups the difference was significant (
p
<
0.001). Analyzing the relationship of
K
i values to time-points, we observed a trend towards a decrease over time (
r
=
−
0.61,
p
=
0.014). Both ADC values (
r
=
−
0.58,
p
=
0.02) and ischemic lesion volumes (
r
=
0.75,
p
=
0.0015) correlated with
K
i values. These results suggest that after ischemia–reperfusion in rats, BBB leakage is continuous during a 4-week period. Its magnitude diminishes over time and correlates with severity and extent of ischemic injury.
Hypertension is one of the strongest risk factors for stroke in the general population, while systolic blood pressure has been shown to independently increase the risk of stroke in type 1 diabetes. ...The aim of this study was to elucidate the association between different blood pressure variables and risk of stroke in type 1 diabetes, and to explore potential nonlinearity of this relationship.
We included 4105 individuals with type 1 diabetes without stroke at baseline, participating in the nationwide Finnish Diabetic Nephropathy Study. Mean age at baseline was 37.4 ± 11.9 years, median duration of diabetes 20.9 (interquartile range 11.5-30.4) years, and 52% were men. Office systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured. Based on these pulse pressure (PP) and mean arterial pressure (MAP) were calculated. Strokes were classified based on medical and autopsy records, as well as neuroimaging. Cox proportional hazard models were performed to study how the different blood pressure variables affected the risk of stroke and its subtypes.
During median follow-up time of 11.9 (9.21-13.9) years, 202 (5%) individuals suffered an incident stroke; 145 (72%) were ischemic and 57 (28%) hemorrhagic. SBP, DBP, PP, and MAP all independently increased the risk of any stroke. SBP, PP, and MAP increased the risk of ischemic stroke, while SBP, DBP, and MAP increased the risk of hemorrhagic stroke. SBP was strongly associated with stroke with a hazard ratio of 1.20 (1.11-1.29)/10 mmHg. When variables were modeled using restricted cubic splines, the risk of stroke increased linearly for SBP, MAP, and PP, and non-linearly for DBP.
The different blood pressure variables are all independently associated with increased risk of stroke in individuals with type 1 diabetes. The risk of stroke, ischemic stroke, and hemorrhagic stroke increases linearly at blood pressure levels less than the current recommended treatment guidelines.
BACKGROUND AND PURPOSE—Admission hyperglycemia is associated with poor clinical outcome in ischemic and hemorrhagic stroke. Admission hyperglycemia has not been investigated in patients with cerebral ...venous thrombosis.
METHODS—Consecutive adult patients with cerebral venous thrombosis were included at the Academic Medical Center, The Netherlands (2000–2014) and the Helsinki University Central Hospital, Finland (1998–2014). We excluded patients with known diabetes mellitus and patients without known admission blood glucose. We defined admission hyperglycemia as blood glucose ≥7.8 mmol/L (141 mg/dL) and severe hyperglycemia as blood glucose ≥11.1 mmol/L (200 mg/dL). We used logistic regression analysis to determine if admission hyperglycemia was associated with modified Rankin Scale (mRS) score of 3 to 6 or mortality at last follow-up. We adjusted forage, sex, coma, malignancy, infection, intracerebral hemorrhage, deep cerebral venous thrombosis, and location of recruitment.
RESULTS—Of 380 patients with cerebral venous thrombosis, 308 were eligible. Of these, 66 (21.4%) had admission hyperglycemia with 8 (2.6%) having severe admission hyperglycemia. Coma (31.3% versus 5.0%, P<0.001) and intracerebral hemorrhage (53.0% versus 32.6%, P=0.002) at presentation were more common among patients with admission hyperglycemia than normoglycemic patients. Patients with admission hyperglycemia had a higher risk of mRS score of 3 to 6 (adjusted odds ratio, 3.10; 95% confidence interval, 1.35–7.12) and mortality (adjusted odds ratio, 4.13; 95% confidence interval, 1.41–12.09). Severe hyperglycemia was even more strongly associated with mRS score of 3 to 6 (adjusted odds ratio, 11.59; 95% confidence interval, 1.74–77.30) and mortality (adjusted odds ratio, 33.36; 95% confidence interval, 3.87–287.28) compared with normoglycemic patients.
CONCLUSIONS—Admission hyperglycemia is a strong predictor of poor clinical outcome in patients with cerebral venous thrombosis.
BACKGROUND AND PURPOSE—Simultaneous multiple intracerebral hemorrhages (SMICHs) are uncommon. Few single-center studies have analyzed characteristics and outcome of SMICH. We analyzed clinical ...characteristics and outcome of SMICH patients from 2 comprehensive stroke centers.
METHODS—Baseline imaging from consecutive intracerebral hemorrhage (ICH) patients (n=1552) from Helsinki ICH study and Royal Melbourne Hospital ICH study was screened for SMICH. ICH pathogenesis was classified according to the structural lesion, medication, amyloid angiopathy, systemic/other disease, hypertension, undetermined classification system (SMASH-U). ICH caused by trauma, tumor, and aneurysmal rupture was excluded. Baseline clinical and radiological characteristics and 90-day mortality were compared between SMICH and single ICH patients. Association of SMICH with 90-day mortality was assessed in multivariable logistic regression models adjusted for predictors of ICH outcome.
RESULTS—Of 1452 patients, 85 (5.9%) were classified as SMICH. SMICH were more often female (58% versus 42%; P=0.004), had lower baseline Glasgow Coma Scale (12 versus 14; P=0.008), and more frequent lobar location (59% versus 34%; P<0.001) compared with single ICH. The SMASH-U pathogenesis of SMICH patients was less often hypertensive (20% versus 37%; P=0.001), more often systemic coagulopathy (12% versus 3%; P<0.001), and trended toward more cerebral amyloid angiopathy (32% versus 23%; P=0.071). SMICH was not associated with 90-day mortality on univariate (37% versus 35%; P=0.610), multivariable (odds ratio, 0.783; 95% confidence interval, 0.401–1.529; P=0.473), or propensity score–matched analyses (odds ratio, 0.760; 95% confidence interval, 0.352–1.638; P=0.484).
CONCLUSIONS—SMICH occurs in ≈1 in 20 ICH, more commonly with lobar located hematomas and systemic coagulopathy with less hypertensive angiopathy. The associated mortality is similar to single ICH. Given varied etiologies, SMICH management should target the underlying pathology.
Highlights ► Motor cortex excitability, modulated by afferent input, is increased in the affected hemisphere in the acute phase after stroke and decreases subsequently during recovery. ► Motor cortex ...excitability correlates with strength of secondary somatosensory cortex (SII) activation, suggesting that modulatory afferent input may reach the motor cortex via SII. ► Afferent input modulated motor cortex excitability is associated with hand function, underlining the importance of parallel recovery of the sensory and motor systems for normal hand dexterity.
Aims
To determine if medium- and long-term blood glucose control as well as glycemic variability, which are known to be strong predictors of vascular complications, are associated with underlying ...cerebral small vessel disease (cSVD) in neurologically asymptomatic individuals with type 1 diabetes.
Methods
A total of 189 individuals (47.1% men; median age 40.0, IQR 33.0–45.2 years) with type 1 diabetes (median diabetes duration of 21.7, IQR 18.3–30.7 years) were enrolled in a cross-sectional retrospective study, as part of the Finnish Diabetic Nephropathy (FinnDiane) Study. Glycated hemoglobin (HbA
1c
) values were collected over the course of ten years before the visit including a clinical examination, biochemical sampling, and brain magnetic resonance imaging. Markers of glycemic control, measured during the visit, included HbA
1c
, fructosamine, and glycated albumin.
Results
Signs of cSVD were present in 66 (34.9%) individuals. Medium- and long-term glucose control and glycemic variability did not differ in individuals with signs of cSVD compared to those without. Further, no difference in any of the blood glucose variables and cSVD stratified for cerebral microbleeds (CMBs) or white matter hyperintensities were detected. Neither were numbers of CMBs associated with the studied glucose variables. Additionally, after dividing the studied variables into quartiles, no association with cSVD was observed.
Conclusions
We observed no association between glycemic control and cSVD in neurologically asymptomatic individuals with type 1 diabetes. This finding was unexpected considering the large number of signs of cerebrovascular pathology in these people after two decades of chronic hyperglycemia and warrants further studies searching for underlying factors of cSVD.
Amplitude or frequency alterations of spontaneous brain oscillations may reveal pathological phenomena in the brain or predict recovery from brain lesions, but the temporal evolution and the ...functional significance of these changes is not well known. We performed follow-up recordings of spontaneous brain oscillations with whole-head MEG in 16 patients with first-ever stroke in the middle cerebral artery territory, affecting upper limb motor function, 1-7 days (T0), 1 month (T1), and 3 months (T2) after stroke, with concomitant clinical examination. Clinical test results improved significantly from T0 to T1 or T2. During recovery (at T1 and T2), the strength of temporo-parietal ≈ 10-Hz oscillations in the affected hemisphere (AH) was increased as compared with the unaffected hemisphere. Abnormal low-frequency magnetic activity (ALFMA) at ≈ 1 Hz in the AH was detected in the perilesional cortex in seven patients at T0. In four of these, ALFMA persisted at T2. In patients with ALFMA, the lesion size was significantly larger than in the rest of the patients, and worse clinical outcome was observed in patients with persisting ALFMA. Our results indicate that temporo-parietal ≈ 10-Hz oscillations are enhanced in the AH during recovery from stroke. Moreover, stroke causes ALFMA, which seems to persist in patients with worse clinical outcome.
Post-thrombectomy intracranial hemorrhages (PTIH) are dangerous complications of acute ischemic stroke (AIS) following mechanical thrombectomy. We aimed to investigate if S100b levels in AIS clots ...removed by mechanical thrombectomy correlated to increased risk of PTIH.
We analyzed 122 thrombi from 80 AIS patients in the RESTORE Registry of AIS clots, selecting an equal number of patients having been pre-treated or not with rtPA (40 each group). Within each subgroup, 20 patients had developed PTIH and 20 patients showed no signs of hemorrhage. Gross photos of each clot were taken and extracted clot area (ECA) was measured using ImageJ. Immunohistochemistry for S100b was performed and Orbit Image Analysis was used for quantification. Immunofluorescence was performed to investigate co-localization between S100b and T-lymphocytes, neutrophils and macrophages. Chi-square or Kruskal-Wallis test were used for statistical analysis.
PTIH was associated with higher S100b levels in clots (0.33 0.08-0.85 vs. 0.07 0.02-0.27 mm
, H1 = 6.021,
= 0.014
), but S100b levels were not significantly affected by acute thrombolytic treatment (
= 0.386). PTIH was also associated with patients having higher NIHSS at admission (20.0 17.0-23.0 vs. 14.0 10.5-19.0, H1 = 8.006,
= 0.005) and higher number of passes during thrombectomy (2 1-4 vs. 1 1-2.5, H1 = 5.995,
= 0.014
). S100b co-localized with neutrophils, macrophages and with T-lymphocytes in the clots.
Higher S100b expression in AIS clots, higher NIHSS at admission and higher number of passes during thrombectomy are all associated with PTIH. Further investigation of S100b expression in AIS clots by neutrophils, macrophages and T-lymphocytes could provide insight into the role of S100b in thromboinflammation.
The relationship between baseline perihematomal edema (PHE) and inflammation, and their impact on survival after intracerebral hemorrhage (ICH) are not well understood.
Assess the association between ...baseline PHE, baseline C-reactive protein (CRP), and early death after ICH.
Analysis of pooled data from multicenter ICH registries. We included patients presenting within 24 h of symptom onset, using multifactorial linear regression model to assess the association between CRP and edema extension distance (EED), and a multifactorial Cox regression model to assess the association between CRP, PHE volume and 30-day mortality.
We included 1,034 patients. Median age was 69 (interquartile range IQR 59-79), median baseline ICH volume 11.5 (IQR 4.3-28.9) mL, and median baseline CRP 2.5 (IQR 1.5-7.0) mg/L. In the multifactorial analysis adjusting for cohort, age, sex, log-ICH volume, ICH location, intraventricular hemorrhage (IVH), statin use, glucose, and systolic blood pressure, baseline log-CRP was not associated with baseline EED: for a 50% increase in CRP the difference in expected mean EED was 0.004 cm (95%CI 0.000-0.008,
= 0.055). In a further multifactorial analysis, after adjusting for key predictors of mortality, neither a 50% increase in PHE volume nor CRP were associated with higher 30-day mortality (HR 0.97; 95%CI 0.90-1.05,
= 0.51 and HR 0.98; 95%CI 0.93-1.03,
= 0.41, respectively).
Higher baseline CRP is not associated with higher baseline edema, which is also not associated with mortality. Edema at baseline might be driven by different pathophysiological processes with different effects on outcome.
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