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The objective was to assess the effect of hard martial arts on the physical fitness components such as balance, flexibility, gait, strength, cardiorespiratory function and several mental functions in people over forty. A computerized literature search was carried out. Studies were selected when they had an experimental design, the age of the study population was >40, one of the interventions was a hard martial art, and when at least balance and cardiorespiratory functions were used as an outcome measure. We included four studies, with, in total, 112 participants, aged between 51 and 93 years. The intervention consisted of Taekwondo or Karate. Total training duration varied from 17 to 234 h. All four studies reported beneficial effects, such as improvement in balance, in reaction tests, and in duration of single leg stance. We conclude that because of serious methodological shortcomings in all four studies, currently there is suggestive, but insufficient evidence, that hard martial arts practice improves physical fitness functions in healthy people over 40. However, considering the importance of such effects, and the low costs of the intervention, the potential of beneficial health effects of age-adapted, hard martial arts training, in people over 40, warrants further study.

Enlarged Virchow-Robin spaces (EVRS) are considered to be a sign of cerebral small vessel disease. Hypertension is an important risk factor for cerebral small vessel disease, whereas ambulatory blood pressure (BP) is the strongest predictor of hypertension-related brain damage. However, the association between ambulatory BP levels and EVRS has never been investigated. The aim of this study was to determine the association between ambulatory BP levels and EVRS. In 143 first-ever lacunar stroke patients, we performed 24-h ambulatory BP monitoring after the acute stroke phase. On brain MRI we counted EVRS in the basal ganglia and the centrum semiovale. We graded the number of EVRS at each level into a three-category severity scale. We assessed the association between BP levels and EVRS by ordinal regression analysis. After adjusting for age, sex, extensive white matter lesions, and asymptomatic lacunar infarcts, higher day systolic (OR 1.21; 95 % CI 1.00-1.46 per 10 mmHg), day diastolic (1.18; 95 % CI 1.02-1.37 per 5 mmHg) and 24-h diastolic (OR 1.18; 95 % CI 1.01-1.37 per 5 mmHg) ambulatory BP levels were associated with EVRS at the basal ganglia level. No relation was found between ambulatory BP levels and EVRS in the centrum semiovale. Higher day ambulatory BP levels are associated with EVRS in the basal ganglia. This association was independent of the presence of extensive white matter lesions and asymptomatic lacunar infarcts. Our results imply that basal ganglia EVRS should be regarded as a separate manifestation of BP-related brain damage.

Objectives: New insights in the pathophysiology of lacunar stroke (LS) suggest that it is caused by increased permeability of the blood-brain barrier due to endothelial activation. Because endothelial cells are the major production and storage site of tissue factor pathway inhibitor (TFPI), this protein can be used as marker of endothelial activation. In this observational study we measured the different pools of TFPI, as a marker of endothelial function, in first-ever lacunar stroke patients. Methods: We determined antigen levels of total and free full-length (FL) TFPI using ELISA in 149 patients and 42 controls. Heparin-releasable free FL TFPI was determined in a random subset of 17 patients and 15 controls. By brain MRI, we classified LS patients as having isolated lacunar infarct (ILA) or silent ischemic lesions (SILs). Results: Plasma levels of total TFPI were highest in patients with SILs compared with those with ILA, but this association disappeared after correction for age and levels of low-density lipoprotein cholesterol. However, levels of heparin-releasable free FL TFPI were higher in patients than in controls. Conclusions: Although ambient plasma levels of total TFPI were not different in subtypes of LS, the increased levels of heparin-releasable TFPI in patients suggest a role of endothelial activation in the pathogenesis of LS. Neurology (R) 2012;78:493-498

Background and Purpose— Cerebral small vessel disease (CSVD) may be caused by endothelial dysfunction, whereas endothelial progenitor cells (EPC) may attenuate endothelial dysfunction. Their vitality is lower in CSVD. A subset of lymphocytes, angiogenic T-cells, is capable to stimulate EPC function. The purpose of our study was to explore the relation between CSVD manifestations, angiogenic T-cells, and EPC in hypertensive patients with CSVD. Methods— We compared 32 essential hypertensive patients with CSVD (white matter lesions, asymptomatic lacunar infarcts, or microbleeds on 1.5-Tesla MRI) to 29 age-matched and sex-matched hypertensive controls. We counted angiogenic T-cells (CD3 + /CD31 + /CD184 + ) and putative EPC (CD31 + /CD34 + /CD45 - /KDR + ) by flow cytometry and determined EPC vitality by in vitro cluster formation. Results— Putative EPC numbers were lower in hypertensive individuals with CSVD than in those without (10±7 . 10 3 /mL versus 13±6 . 10 3 /mL [median±interquartile range]; P =0.011). Angiogenic T-cell numbers were also lower in hypertensive individuals with CSVD than in those without (0.56±0.25 . 10 9 /mL versus 0.78±0.50 . 10 9 /mL; P =0.008). Higher angiogenic T-cell numbers independently related to absence of CSVD (odds ratio, 0.088; 95% confidence interval, 0.012–0.627). Conclusions— Our data suggest that angiogenic T-cells and putative EPC independently relate to radiological CSVD manifestations in hypertensive patients.

Background and Purpose— Results from case-control and case-case studies indicate that a positive family history of stroke (FHstroke) is an independent risk factor for lacunar stroke. Different lacunar stroke phenotypes can be distinguished on the basis of the presence of asymptomatic lacunar infarcts (aLACs), ischemic white-matter lesions, or brain microbleeds. The aim of the present study was to determine whether familial aggregation of stroke was different for lacunar stroke phenotypes. Methods— In 157 patients with a first-ever lacunar stroke, a complete first-degree FHstroke was obtained by a standardized questionnaire and additional interview. Lacunar stroke patients were categorized successively into groups, depending on the presence of aLACs, ischemic white-matter lesions, and brain microbleeds on magnetic resonance imaging. Results— Fifty-two percent of patients reported a positive FHstroke in at least one of their first-degree relatives. In younger (P Conclusions— A family history of stroke might be an independent risk factor for the lacunar stroke phenotype with aLACs at younger ages, suggesting a role for genetic factors in this phenotype caused by diffuse vasculopathy.

Contains fulltext : 87253.pdf (Publisher’s version ) (Closed access) The presence of Chlamydia pneumoniae in murine brain tissue was studied in atherosclerotic and non-atherosclerotic mice, after peritoneal injection. Furthermore, we investigated whether increased permeability of the blood-brain barrier was implicated in cerebral C. pneumoniae infection and whether intra-cerebral C. pneumoniae infection leads to microglial activation. Using a polymerase chain reaction, C. pneumoniae DNA was found in the brain tissue of 33% of the mice, 3, 7 and 21 days after infection. Atherosclerosis and age does not influence the extend of the cerebral infection. Semiquantitative analyses showed that intra-cerebral C. pneumoniae infection was not accompanied by an altered function of the blood-brain barrier. Microglial activation was assessed with immunohistochemistry, quantified in the hippocampus of each infected mouse and compared with mock infected. Enhanced microglial activation was found in the atherosclerotic mice. Since microglial activation is a key factor in a number of neuroinflammatory diseases, C. pneumoniae infection might play a role in these diseases. 01 oktober 2010

Background: Metabolic syndrome (MetS) is a cluster of three or more of the following risk factors: obesity, elevated blood pressure, elevated triglyceride level, elevated glucose level, and low high-density lipoprotein level. Lacunar infarcts (LS) account for 25% of all ischemic strokes and are small, deeply located brain infarcts. Two different subtypes exist, which are distinguished by the presence of concomitant white matter lesions (WML) on brain imaging. We determined the prevalence of MetS in LS and the association between MetS with LS subtypes in a series of first-ever LS patients. Methods: We included 92 patients with a first-ever LS, and 92 patients with a first-ever atheroslerotic cortical stroke (CS) matched for age and sex. LS subtypes were defined according to presence of concomitant WML. We defined MetS retrospectively according to previously defined standards. Results: 35.9% of LS patients and 45.7% of CS patients had MetS (OR 0.67; 95% CI 0.37–1.20). MetS was more prevalent in LS without WML than in LS with WML (44.4 and 23.7%, respectively; OR 2.98; 95% CI 1.04–8.47). Similarly, MetS related more to CS compared to LS with WML (OR 2.56; 95% CI 1.03–6.37). Conclusion: MetS relates more strongly to LS without WML and to CS, than to LS with WML. Our results suggest a different underlying mechanism between LS without WML and CS, and lacunar stroke with WML.

Background and Purpose— Hypertension is an important risk factor for brain microbleeds (BMBs) in lacunar stroke patients. However, beyond the qualitative label “hypertension,” little is known about the association with ambulatory blood pressure (BP) levels. Methods— In 123 first-ever lacunar stroke patients we performed 24-hour ambulatory BP monitoring after the acute stroke-phase. We counted BMBs on T2*-weighted gradient-echo MR images. Because a different etiology for BMBs according to location has been suggested, we distinguished between BMBs in deep and lobar location. Results— BMBs were seen in 36 (29.3%) patients. After adjusting for age, sex, number of antihypertensive drugs, asymptomatic lacunar infarcts, and white matter lesions, we found 24-hour, day, and night systolic and diastolic BP levels to be significantly associated with the presence and number of BMBs (odds ratios 1.6 to 2.3 per standard deviation increase in BP). Distinguishing between different locations, various BP characteristics were significantly associated with the presence of deep (or combined deep and lobar) BMBs, but not with purely lobar BMBs. Conclusions— Our results underline the role of a high 24-hour BP load as an important risk factor for BMBs. The association of BP levels with deep but not purely lobar BMBs is in line with the idea that different vasculopathies might be involved. Deep BMBs may be a particular marker of BP-related small vessel disease, but longitudinal and larger studies are now warranted to substantiate these findings.

High daytime and nighttime blood pressure (BP) levels, and apparently also an abnormal nocturnal BP dip, coincide with a greater extent of cerebral white matter hyperintensities (WMHs). We assessed the relationship between ambulatory BP and volumes of WMH, and distinguished between periventricular and deep WMH because of their supposedly different cause.A total of 210 hypertensive patients (106 men) without cardiovascular and cerebrovascular disease, with a mean age of 52.5 +/- 12.5 years, and untreated office BP levels of 170 +/- 24/104 +/- 12 mmHg underwent duplicate 24-h ambulatory blood pressure monitoring (off medication) and brain MRI to quantify the WMHs (total, periventricular, and deep) and brain volumes. We performed linear regression analyses to relate the mean 24-h, awake, and asleep BPs, and the relative nocturnal BP dip to the different volumes of WMHs, while adjusting for age, sex, brain volume, and vascular risk factors.Higher 24-h, awake, and asleep BP levels were continuously, without distinct thresholds, and independently associated with a greater volume of total (all P0.001), periventricular (P0.001), and, to a lesser extent, deep (P0.05) WMHs. Nocturnal BP dipping was not related to the volume of WMHs.Higher 24-h, daytime, and nighttime BP levels are independently associated with WMH volumes.

Background and Purpose— Blood–brain barrier dysfunction may be an early phenomenon in the development of the small vessel disease, which underlies white matter lesions. Because vitamin B12 plays a role in maintaining the integrity of the blood–brain barrier, we studied serum vitamin B12 level in relation to such lesions. Methods— In 124 patients with first lacunar stroke, we measured serum vitamin B12 level and rated the degree of white matter lesions on MRI. Results— Mean vitamin B12 level was 202 pmol/L (SD, 68.9). Thirty-nine patients (31.5%) had a vitamin B12 level less than the lower reference value of 150 pmol/L. Lower vitamin B12 level was (statistically significant) associated with more severe periventricular white matter lesions (odds ratio/100 pmol/L decrease, 1.773; 95% CI, 1.001–3.003), but not with deep white matter lesions (odds ratio/100 pmol/L decrease, 1.441; 95% CI, 0.881–2.358; ordered multivariate regression analysis). Conclusions— More severe periventricular white matter lesions in lacunar stroke patients relate to lower vitamin B12 levels. A possible causal relationship should now be studied prospectively.

Detection of preclinical hypertension-related cardiorenal damage has been recommended in the identification of patients most at risk of cardiovascular complications. The inclusion of silent cerebrovascular disease (SCD) as an additional marker of hypertensive organ involvement might improve risk stratification.In 192 hypertensive patients (98 men) without a history of cardiovascular and cerebrovascular disease, a mean age of 51.6 +/- 12.3 years and untreated office blood pressure levels of 170 +/- 23/104 +/- 12 mmHg, we obtained detailed information on preclinical cardiac (left ventricular hypertrophy), renal (microalbuminuria, impaired kidney function or both) and cerebrovascular damage (white matter hyperintensities, infarcts, microbleeds or all), and estimated the associated cardiovascular risk on the basis of the presence of common cardiovascular risk factors.Hypertensive target-organ damage involved the heart in 41 (21%), the kidneys in 50 (26%) and the brain in 84 (44%) participants. When considering only patients with demonstrable cardiac, renal damage or both (n = 72), 42 participants (58%) had also SCD. Of the remaining 120 participants without cardiorenal damage, 42 (35%) had brain damage. In other words, half of all patients with SCD were classified as having no target-organ (i.e., cardiorenal) involvement. The cardiovascular risk score of patients without cardiorenal but with brain damage was significantly higher than that of participants without any organ involvement (37 +/- 11 versus 27 +/- 11, P0.001), and similar to the risk score of those with cardiorenal damage (38 +/- 14, P0.05).These data suggest that SCD should be recognized as an additional, independent and prognostically relevant marker of preclinical hypertensive target-organ damage.

Cerebral small vessel disease results in silent ischemic lesions (SIL) among which is leukoaraiosis. In this process, endothelial damage is probably involved. Endothelial progenitor cells (EPC), are involved in endothelial repair. By restoring the damaged endothelium, EPC could mitigate SIL and cerebral small vessel disease. Haptoglobin 1-1, one of three phenotypes of haptoglobin, relates to SIL and may therefore attenuate the endothelial repair by EPC. Our aim was to quantify EPC number and function and to assess haptoglobin phenotype and its effect on EPC function in patients with a high prevalence of SIL: lacunar stroke patients. We assessed EPC In 42 lacunar stroke patients and 18 controls by flow cytometry and culture with fetal calf serum, patient and control serum. We determined haptoglobin phenotype and cultured EPC with the three different haptoglobin phenotypes. We found that EPC cluster counts were lower in patients (96.9 clusters/well +/- 83.4 (mean +/- SD)), especially in those with SIL (85.0 +/- 64.3), than in controls (174.4 +/- 112.2). Cluster formation was inhibited by patient serum, especially by SIL patient serum, but not by control serum. Patients with haptoglobin 1-1 had less clusters in culture, and when haptoglobin 1-1 was added to EPC cultures, cluster numbers were lower than with the other haptoglobin phenotypes. We conclude that lacunar stroke patients, especially those with SIL, have impaired EPC cluster formation, which may point at decreased endothelial repair potential. The haptoglobin 1-1 phenotype is likely a causative factor in this impairment.

Background: Endothelial dysfunction is thought to play an important role in the pathogenesis and progression of cerebral small-vessel disease in lacunar stroke patients. Methods: We systematically searched the literature (MEDLINE, EMBASE) for evidence of endothelial activation and dysfunction in lacunar stroke. The selected papers were assessed by a predefined checklist to estimate methodological and informative quality. The papers were categorized into subheadings concerning the different physiologic functions of the endothelium and a subheading concerning toxins for the endothelium. Results: 29 articles were eligible for further analysis. We found 16 publications on regulation of vascular tone by the endothelium, which showed an impaired function at several time points after the stroke by means of different clinical methods (e.g. flow-mediated vasodilatation and CO2 reactivity). Nine references showed elevated levels of markers of hemostatic function of the vascular endothelium (e.g. von Willebrand factor, thrombomodulin) in acute and subsequent phases. In 4 papers, adhesion molecules (e.g. E- and P-selectin) were elevated only during the acute phase. Homocysteine, a toxin for the endothelium, was elevated in patients in 3 papers. Conclusions: The current literature suggests that endothelial dysfunction might be involved in the pathogenesis of lacunar stroke, especially in those patients with concomitant silent lacunar infarcts and ischemic white matter lesions. Future research on endothelial function in lacunar stroke should concentrate on long-term clinical as well as radiological follow-up in well-defined cases and combine multiple methods to evaluate endothelial function.

Haptoglobin (Hp) 2-2 phenotype has been associated with peripheral and coronary artery disease and risk of vascular complications in diabetic patients, but any association of Hp polymorphism with cerebrovascular disease has not been explored so far. We aimed to study Hp polymorphism in a sample of 124 patients with a rather homogeneous type of cerebrovascular disease, namely first symptomatic lacunar stroke due to small vessel disease, in comparison with a large (n=918) control group. Hp phenotypes were determined using starch gel electrophoresis. Hp1 allele frequency was significantly higher in patients than in controls (0.480 vs. 0.395, p < 0.05), mainly due to a lower Hp2-2 phenotype frequency (25.0 vs. 36.3 %; OR 0.59; 95%CI 0.38-0.90; p < 0.05). This was even more pronounced in younger (60 years) patients (Hp1 allele frequency 0.539). Concomitant asymptomatic lacunar lesions were present in 82 patients, extensive white matter lesions in 47 patients. The association between Hp1 and lacunar stroke suggests that Hp may serve different functions depending on the pathological processes in various types of vascular disease in different organs. The association between Hp1 and lacunar stroke may relate to blood-brain barrier dysfunction, to the association between hypertension and cerebral small vessel disease, or a special dependence of small vessel wall integrity on Hp2-2 related angiogenic potential. The presence of concomitant signs of cerebral small vessel disease weakened the association between Hp1 and lacunar stroke, which could reflect a difference in underlying vascular pathophysiology in which Hp phenotype may play a different role.

Background and Purpose— Stroke is the leading cause of disability in the Western world; however, few therapies are at hand to decrease this burden. Summary of Review— Endothelial progenitor cells (EPCs) have been introduced in cardiovascular medicine as factotums. EPCs can repair damaged endothelium and attenuate the development and progression of atherosclerosis. Also, EPCs can form new vessels in ischemic areas and thus promote recovery after ischemic events. In stroke, however, EPC research is limited. In our overview, we provide background information on EPC use as a risk marker and as a potential therapeutic agent. Conclusion— In our opinion, the lack of EPC studies in stroke should instigate vascular neurologists to participate in EPC research, as EPCs could also change pathophysiological concepts and improve clinical treatments in vascular neurology.

Contains fulltext : 69494.pdf (Publisher’s version ) (Open Access) Aims: To explore whether Chlamydia pneumoniae, Cytomegalovirus and Herpes Simplex Virus type 1 could be detected in large and small cerebral arteries, as well as in an area of brain parenchyma where white matter lesions (leukoaraiosis) can be found, in patients with clinically unmanifested cerebrovascular atherosclerosis. Methods and results( Arterial specimens from the basilar artery and middle cerebral artery, and brain samples from the basal ganglia and periventricular white matter were obtained. Neuropathological changes were assessed in Haematoxylin-Eosin stained sections. Polymerase chain reaction (PCR) was performed on paraffin embedded sections. Subsequently, we performed immunohistochemical staining on samples, which were found positive in PCR. We failed to detect C. pneumoniae, CMV, or HSV-1, in any of the cerebral large vessels. In the brain tissue, we found only one case positive for CMV, and one for C. pneumoniae. Conclusions (our findings suggest a limited role for C. pneumoniae, CMV and HSV-1 in cerebral large and small vessel atherosclerosis.

Objective We assessed how different definitions of the awake and asleep periods and use of various blood pressure (BP) indices affect the extent of the nocturnal BP dip, the prevalence of dippers and nondippers, their respective reproducibilities and the relation of nondipping with target-organ damage. Methods We performed 24-h ambulatory BP monitoring twice and determined the left ventricular mass index and urinary albumin excretion as indices of target-organ damage in 150 hypertensive patients (off-medication). Awake and asleep periods were assessed using fixed and diary time methods, covering all readings available (wide) or excluding morning and evening transition hours (narrow). Nondipping (BP dip < 10%) was established for systolic BP and diastolic BP, their combinations (and/or), and mean arterial pressure. Results The different awake-asleep definitions caused significant variation in both the extent of the BP dip and the number of dippers and nondippers in comparison with the wide diary definition (i.e. use of actual awake and sleep periods). The prevalences of dippers and nondippers also varied significantly with the BP index. Reproducibility analyses of the BP dip and the dipping status yielded repeatability coefficients (expressed as percentages of nearly maximal variation) between 42.39 and 48.71%, and kappa values between 0.323 and 0.459, respectively. Some classifications, but not all, discriminated significantly between consistent dippers and nondippers in terms of left ventricular mass index or urinary albumin excretion. Conclusions Use of different definitions of awake-asleep and BP indices affects significantly the classification of nocturnal BP dipping and its relation with hypertensive target-organ damage.

Brain microbleeds, indicative of cerebral small-vessel disease, may occur with increased frequency in patients with hypertension. However, little is known about the relation of these abnormalities with blood pressure levels. We assessed the relation between ambulatory measured blood pressure and the presence of microbleeds in a cohort of hypertensive patients without a history of cerebrovascular disease. A total of 218 participants (110 males, age 52.5±12.6 years) underwent 24-hour ambulatory blood pressure monitoring twice (off-medication) and brain MRI to detect microbleeds and coexisting white matter hyperintensities. We performed logistic regression analyses to relate the following blood pressure components (based on both recordings) to microbleeds: the mean 24-hour, awake, and asleep blood pressures; nocturnal hypertension (asleep pressure ≥120/70 mm Hg); nocturnal blood pressure dipping. Models were adjusted for age and sex, and additionally for cardiovascular risk factors and white matter hyperintensities. We detected microbleeds in 35 participants (16.1%; 95% confidence interval, 11.1% to 21.0%). On average, each standard deviation increment in blood pressure, whether 24-hour, awake, or asleep, was significantly and independently associated with a 1.8- to 1.9-fold higher likelihood for microbleeds (all models P P

Background: Mortality studies in lacunar (LAC) stroke are scarce and often characterized by short follow-up time, small patient groups and absence of a nonlacunar stroke group for comparison. Besides, there are no separate long-term prognostic data on LAC stroke subtypes. We performed a long-term mortality study in LAC stroke, subtyping two distinct phenotypes and including nonlacunar ischemic stroke for comparison. Methods: We performedcross-sectional follow-up, determining survival status, after a median of 15.0 years, in 333 first-ever atherothrombotic (AT), 184 cardioembolic (CE) and 265 LAC strokes, distinguishing LAC stroke with (type 2) or without (type 1) asymptomatic LAC lesions on CT. Results: End of follow-up mortality (in 30-day survivors) in LAC stroke (76.2%) was significantly lower than in CE (87.1%; OR 0.48, 95% CI 0.27–0.84), but not AT strokes (79.0%; OR 0.85, 95% CI 0.57–1.26), and was significantly lower in LAC type 1 than type 2 strokes (70.9 vs. 87.5%; OR 0.35, 95% CI 0.17–0.73). Kaplan-Meier analysis showed most favorable survival in LAC type 1 stroke. In the Cox regression analyses, LAC type 1 strokeappearedas an independent predictor of better survival versus LAC type 2, versus AT and versus CE strokes. Conclusions: LAC stroke in general cannot be considered a ‘benign’ stroke type: only long-term survival in patients without concomitant asymptomatic LAC lesions is better than in large-vessel stroke. This difference in long-term survival between the two LAC stroke subtypes should be taken into account in prognostic counselling of individual LAC stroke patients.

Although ample research has been done into cognitive disorders occurring after stroke, relatively few data are available on the development and the course of vascularmild cognitive impairment (VMCI) after first-ever lacunar stroke. Methods: A cohort of 95 patients with a first-ever symptomaticlacunar infarct, older than 40 years, MMSE ≧15 and no other neurological or major psychiatric deficits were included. Patients were assessed (clinically and with a neuropsychological test battery) at 1 and 24 months after stroke, and CT was repeated. VMCI was diagnosed when patients had a deficit in at least one cognitive domain, in the absence of dementia. Results: Approximately 75% of the patients had VMCI at 1 month; this percentage was somewhat lower at 2 years. Only initial stroke severity was an independent predictor of VMCI after stroke. Conclusion: VMCI is highly prevalent after lacunar stroke, but does not increase during the first 2 years thereafter.

Background: Post-stroke depression (PSD) frequently complicates stroke and is associated with an impaired functional outcome, more severe cognitive deficits, a reduced quality of life, and a higher mortality. The aim of this study was to assess whether general risk factors for major depressive disorder (MDD) in the community are also risk factors for PSD, and to identify additional, stroke-related risk factors.Methods: In a hospital setting, 190 consecutively admitted patients were assessed for MDD 1 month after stroke, and at follow-up after 3, 6, 9 and 12 months. A Cox model was created with four established risk factors for MDD in the community (female sex, prior personal history of depression, positive family history of depression, and somatic comorbidity other than stroke). Five potential disease-related risk factors (disability, cognitive deterioration, inter- and intrahemispheric lesion location, and generalized vascular damage on computed tomography (CT) scan) were then added individually to this model, to see whether these would improve the significance of the overall model.Results: The Cox model of four general risk factors for depression in the community was shown to be a valid model to predict depression in stroke patients. Of the disease-specific factors, only incorporation of “disability” in this model improved its significance.Conclusion: Established risk factors for depression in the community are also predictors of depression in the first year after stroke. Disability is a non-specific disease-related variable that is associated with PSD. The contribution of stroke-specific factors may be less than is generally assumed.

Background: We tested whether diazepam, a GABA-ergic drug that also inhibits brain nitric monoxide formation, improves acute stroke prognosis. Methods: 880 patients, randomized within 12 h of acute stroke, received diazepam 10 mg or placebo by rectiole, as soon as possible, followed by 10-mg tablets twice daily for 3 days. Primary outcome was independence (Rankin score Results: Intention-to-treat analyses on all 849 patients with full follow-up (50.4% on diazepam): odds ratio (OR) 1.14, 95% CI 0.87–1.49 for primary endpoint, and an OR of 1.26 (0.90–1.76) for complete recovery, both favoring diazepam. Adjusted analyses for all stroke patients (843): OR 1.20 (0.87–1.65), and 1.25 (0.89–1.74), respectively, and for all infarct patients (748): OR 1.31 (0.93–1.85), and 1.46 (1.02–2.09; p = 0.037), respectively. Analyses restricted to cardioembolic infarct patients (200) showed treatment benefit for the primary outcome: OR 2.26, 95% CI 1.07–4.76, p = 0.032, and complete recovery: OR 2.65, 95% CI 1.06–6.59, p = 0.037. About one third of ischemic stroke patients had ‘any adverse event’, without any difference between treatment groups. In 95 intracerebral hemorrhage patients, frequency of pneumonia and death were higher in the diazepam group than in the placebo group: 35 and 10%, 22 and 12%, respectively. Conclusions: Although point estimates favored diazepam treatment in various analyses, our data did not confirm our primary hypothesis. Diazepam treatment seems beneficial in cardioembolic infarct patients, is safe in acute ischemic stroke, but may better be avoided in intracerebral hemorrhage.

Summary Purpose: To estimate the incidence of unprovoked seizures (US) and epilepsy in a general population from the southern part of the Netherlands, in relation to age, sex, etiology and seizure type, and to identify predictive factors of the epileptic and non-epileptic seizures. Methods: All patients aged ≥14 years with a first seizure or who had undiagnosed seizures before the study period were included. Patients were identified from different sources and were independently evaluated and classified by a team of neurologists. A predictive profile for the occurrence of epileptic and non-epileptic seizures was obtained by stepwise logistic regression analysis. Results: The overall annual incidence was 55/100,000 and 30/100,000 for US and epilepsy, respectively. The age-specific annual incidence of US and epilepsy increased with age and reached 120/100,000 and 62/100,000 for the ≥65 years of age group, respectively. The incidence of epilepsy and US in males was higher than in females and partial seizures prevailed over generalized seizures (40 versus 9/100,000). In up to 35% of the cases with US or epilepsy, the etiology was mainly cerebrovascular disease and brain tumors. Predictors for epileptic versus non-epileptic seizures of organic origin were an epileptiform EEG pattern (OR=0.06) versus a history of hypertension (OR=2.8) or cardiovascular disease (OR=5.4). Strong predictors for seizures of non-organic origin were female sex (OR=2.2) and head injury (OR=2.4). Conclusions: The incidence of US and epilepsy (overall, and age-, sex-, seizure-specific) was similar to those reported by other developed countries. The predictive factors found in this study may assist in the early diagnosis of seizures.

There is little agreement about the prevalence and incidence of vascular dementia (VaD) mainly because investigators have used different diagnostic criteria. The aim of this study was to examine the influence of different diagnostic criteria on the prevalence and cumulative incidence of VaD in first-ever stroke patients (n = 194) clinically evaluated at 1, 6, 12, and 24 months after stroke. Post-stroke VaD was diagnosed using the DSM-III, DSM-III-R, DSM-IV, ICD-10-NA, NINDS-AIREN, and ADDTC criteria. The prevalence of dementia was highest at 1 month; ranging from 11.3% with the NINDS-AIREN to 20.1% with the ICD-10-NA. The incidence was highest at 6 months, ranging from 2.6% with the ADDTC to 5.2% with the ICD-10-NA. Agreement among diagnostic criteria was high, with the exception of the ADDTC. In conclusion, both the prevalence and incidence of dementia are highest directly after stroke, but exact rates are influenced by the diagnostic criteria used.

The effect of diazepam on NO-mediated cGMP synthesis was studied in rat brain slices. It was found that diazepam dose-dependently decreased cGMP synthesis in cerebellar slices, with an inhibition of 90% at 1 mM diazepam. cGMP levels in the presence of diazepam were not restored to control levels by the addition of 0.1 mM sodium nitroprusside, whereas the decrease in cerebellar cGMP levels induced by 0.1 mM L-NAME was restored by the simultaneous application of NO-donors. In addition to the decrease of cGMP levels in neuronal structures induced by 1 mM diazepam, we observed increased cGMP immunoreactivity in glial cells in the cerebellum, the hippocampus, and the cerebral cortex. The significance of this observation is discussed.

Background : The Oxfordshire Community Stroke Project (OCSP) classification allows distinction of stroke subtypes with different prognosis. OCSP classification inferred from clinical signs filled out on patient entry forms has been used to facilitate subgroup analysis in clinical trials. However, such procedure has not been validated against clinical diagnosis. In preparation for an acute stroke trial, we set out to perform such a validation. Methods : An OCSP syndrome diagnosis of 194 acute stroke patients in four hospitals was made within 24 h using a standard list with neurological signs, to be filled out by a stroke physician or neurological resident on duty. This was compared with OCSP diagnosis within 2 days of stroke onset by a (blinded) stroke neurologist (‘gold standard’). Results : The proportion of the OCSP syndromes was quite similar between standard list and clinical judgement. Sensitivity, specificity, positive and negative predictive values were respectively: LACS: 0.76, 0.88, 0.72, 0.90; TACS: 0.63, 0.93, 0.62, 0.88; PACS: 0.62, 0.76, 0.63, 0.75; POCS: 0.50, 0.98, 0.60, 0.97. Kappa for agreement was 0.63 (LACS), 0.37 (PACS), 0.50 (TACS). Neuro-imaging falsified stroke subtype diagnosis in 40 cases (20.6%) diagnosed using the standard list, and 42 (21.6%) diagnosed by stroke neurologists. Conclusion : A standard list-derived stroke syndrome diagnosis may be used as a clinical test to make an OCSP syndrome diagnosis in acute stroke. The use of such list in acute stroke trials may facilitate uniformity in early stroke subtype diagnosis. However, to increase such uniformity, ancillary methods such as acute MRI should be evaluated.

The aim of this prospective population-based study was to systematically define a cluster of diagnostic items which can assist in the early identification and classification of epileptic and non-epileptic seizures. A cohort of patients aged ≥14 years, suspected with a first epileptic seizure, were included in this study. A team of neurologists evaluated and classified all cases. Diagnostic items for epileptic and non-epileptic seizures were identified using logistic regression analysis. Three hundred and fifty cases entered this study. Distinctive features for epileptic seizures were postictal confusion (OR 0.09), an epileptiform EEG pattern (OR 0.02), and abnormal neuroimaging findings (OR 0.07), whereas for non-epileptic seizures of organic origin there was a history of hypertension (OR 7.5), and provoking factors (OR 13.4) such as exercise and warmth. Diagnostic items for seizures of non-organic origin were a history of febrile seizures (OR 5.8), treatment by a psychologist or psychiatrist (OR 9.1), and presentiment of the seizure (OR 3.7) such as a feeling of choking and palpitations. A separate analysis for the patients who were systematically investigated provided some additional diagnostic items for the different subgroups of patients. For instance, back arching during the seizure for the patients with seizures of non-organic origin and female sex for the patients with non-epileptic seizures of organic origin.

Aben I, Verhey FRJ, Beusmans G, Lodder J. Depressie na een CVA: signalering, diagnostiek en behandeling in de huisartsenpraktijk. Huisarts Wet 2003;46(9):487-92. Doel Nagaan hoe vaak huisartsen een depressie na een CVA herkennen en behandelen. Methoden In het kader van een prospectief onderzoek werd bij 190 CVA- patienten gedurende 1 jaar iedere 3 maanden nagegaan of zij een depressie hadden volgens de criteria van de DSM-IV. Na afloop van dit jaar werd aan de huisartsen van 58 van hen gevraagd naar diagnostiek en behandeling van depressie bij deze patienten aan de hand van een gestandaardiseerd interview. Resultaten Van de 29 patienten met een depressie volgens DSMIV waren 11 (37,9%) als zodanig door de huisarts gediagnosticeerd. Bij drie patienten werd de diagnose ten onrechte gesteld. Bij de 14 patienten bij wie depressie werd gediagnosticeerd schreef de huisarts in 50% een antidepressivum voor en eveneens in 50% maakten zij een vervolgafspraak. Depressieve patienten bleken veelal hun huisartsen niet voor hun klachten te consulteren. Conclusie Huisartsen herkennen en behandelen een depressie na een CVA vaak niet. Het is noodzakelijk dat patienten die een CVA hebben doorgemaakt goed worden voorgelicht en huisartsen hen stelselmatig controleren op het bestaan van psychische problematiek en daarvoor behandelen of doorverwijzen. Hiervoor zou beleid moeten worden ontwikkeld.

Background and Purpose— Treatment of intracerebral hematoma (ICH) is controversial. An advantage of neurosurgical intervention over conservative treatment of ICH has not been established. Recent reports suggest a favorable effect of stereotactic blood clot removal after liquefaction by means of a plasminogen activator. The SICHPA trial was aimed at investigating the efficacy of this treatment. Methods— A stereotactically placed catheter was used to instill urokinase to liquefy and drain the ICH in 6-hour intervals over 48 hours. From 1996 to 1999, 13 centers entered 71 patients into the study. Patients were randomized into a surgical group (n=36) and a nonsurgical group (n=35). Admission criteria were the following: age >45 years, spontaneous supratentorial ICH, Glasgow Eye Motor score ranging from 2 to 10, ICH volume >10 cm 3 , and treatment within 72 hours. The primary end point was death at 6 months. As secondary end points, ICH volume reduction and overall outcome measured by the modified Rankin scale were chosen. The trial was prematurely stopped as a result of slow patient accrual. Results— Seventy patients were analyzed. Overall mortality at day 180 after stroke was 57%; this included 20 of 36 patients (56%) in the surgical group and 20 of 34 patients (59%) in the nonsurgical group. A significant ICH volume reduction was achieved by the intervention (10% to 20%, P P =0.08). The odds ratio of mortality combined with modified Rankin scale score 5 at 180 days was also not statistically significant (odds ratio, 0.52; 95% confidence interval, 1.2 to 2.3; P =0.38). Conclusions— Stereotactic aspiration can be performed safely and in a relatively uniform manner; it leads to a modest reduction of 18 mL of hematoma reduction over 7 days when compared with control, which has a 7-mL reduction, and therefore may improve prognosis.

This study investigated the occurrence of cognitive disorders 1 and 6 months after stroke in a cohort of patients with a first-ever stroke. In addition, it was investigated whether age, sex and level of education are risk factors for vascular cognitive disorders. Memory, simple speed, cognitive flexibility and overall cognitive functioning were examined in 139 patients at 1 and 6 months post-stroke. Inclusion criteria on admission were first cerebral stroke, age>/=40, no other neurological or psychiatric disorders and ability to communicate. Mean age was 69.3 years (S.D.=12.3). Patients were compared with a healthy control group matched for age, sex and level of education. A large group of patients who, at 1 month after stroke, scored below the cutoff on cognitive domains, scored above the cutoff on most of these cognitive domains at 6 months. For overall cognitive functioning, 16 out of 39, for memory, 13 out of 26 and for cognitive flexibility, 15 out of 49 patients, who at 1 month scored below the cutoff, scored above the cutoff at 6 months. Simple speed did not change; 12 patients scored above the cutoff and 7 patients scored below the cutoff at 6 months after stroke. Speaking in terms of improvement or deterioration, most people remained stable on the four cognitive domains (ranging from 37.6% to 83.5%), and a substantial group improved (ranging from 12.9% to 52.1%). Older and female patients had more cognitive disturbances. Overall, the conclusion is that the prognosis of cognitive functioning after stroke is general favourable, especially in younger patients.

In order to provide tailor-made care, governments are considering the implementation of output-pricing based on hospital case-mix measures, such as diagnosis related groups (DRG). The question is whether the current DRG classification system can provide a satisfactory prediction of the variance of costs in stroke patients and if not, in what way other variables may enhance this prediction. In this study, data from 731 stroke patients hospitalized at University Hospital Maastricht during 1996-1998 are used in the cost analysis. The DRG classification for this group uses information--in addition to the DRG classification operation or no operation--on the patient's age combined with discharge status. The results of regression analysis show that using DRGs, the variance explained in the costs amounts to 34%. Adding other variables to the DRGs, the variance explained increases to about 61%. Additional factors highly correlating with inpatient costs are the level of functioning after stroke, comorbidity, complications, and 'days of stay for non-medical reasons'. Costs decreased for stroke patients discharged during the latter part of the years studied, and if stroke patients happened to die during their hospital stay. The results do suggest that future implementation of output-pricing based on the DRG case-mix measures is feasible for stroke patients only if it is enhanced with information on complications and the level of functioning.

Iwo decades of research have failed to generate consistent insight into the specificity of poststroke depression (PSD). This is, at least in part, caused by methodological difficulties. Differences in symptom profile between PSD and depression with no or another medical cause were described, but no specific and unequivocal clinical picture has been established so far. Prevalence rates of PSD varied largely between studies. In community based studies using standardised diagnostic instruments for depression, relatively low prevalence rates were reported compared to inpatient or rehabilitation studies. PSD occurs most frequently in the first few months after stroke, while a new incidence peak may occur 2-3 years after stroke. Two systematic reviews on the relation between lesion location and depression did not support the claim that left hemisphere lesions are a risk factor for PSD. A new concept of vascular depression has been proposed, which relates depression in the elderly to acute or chronic damage to the cerebral vascular system. Future efforts should aim at increasing the uniformity of study designs, assessment tools should be further improved for use in cognitively impaired patients and appropriate control groups should be defined to study the characteristic features of PSD.

Blood pressure (BP) is often elevated in acute stroke. However, predictors of BP level and BP course during the first week after a stroke remain unknown. Knowledge of such factors may be of relevance when manipulation of early BP levels are considered as potentially therapeutic in acute stroke. In this study, BP data was collected by reviewing BP records of patients who were admitted with a first cerebral infarct to our stroke unit and who had their first BP recordings within 24 hours after stroke onset. Age and known hypertension before stroke were significantly associated with elevated poststroke BP level, whereas ischemic heart disease was associated with a lower BP level. BP decline in the poststroke period related to the initial BP elevation. BP in hypertensive patients remained higher than in nonhypertensive patients during the first poststroke week. Between day 0 and day 4 after stroke onset, only the daytime systolic BP decline showed a significant association with previously established hypertension. There was no difference in initial BP level, nor in the rate of BP decline between day 0 and 4 in patients with a lacunar infarct and those with an infarct involving the cortex. These findings indicate that BP increase poststroke is not a general phenomenon, nor is BP decline in the first poststroke week. Known hypertension is probably the strongest predictor of poststroke BP increase. Hypertensive patients are more sensitive to sympathetic stimulation. Therefore, when lowering of elevated BP early poststroke is tested as a potential neuroprotective modality, it may best be achieved by treating patients with sympathicolytic, antihypertensive drugs. Copyright © 2001 by National Stroke Association

All studies but one in the past have shown a strong relative risk of mitral annulus calcification for stroke, but the contribution of associated cardiac and vascular risk factors, especially carotid atheroma has not been appreciated. We studied the risk of stroke in selected patients with mitral annular calcification, adjusting for clinical, echocardiographic and therapeutic factors influencing stroke risk. Of 8,160 consecutive patients with echocardiograms, 657 with and 562 without mitral annulus calcification were followed for a mean of 2.4 years (range 1-6.6) to determine stroke risk by means of proportional hazards models with clinical, echocardiographic, and therapeutic variables that influence the risk of stroke. We also determined the association of mitral annulus calcification with subtypes of ischaemic brain lesions generally considered to be specific for an underlying cardioembolic cause. We therefore distinguished between territorial, small deep, and asymptomatic (silent) brain infarcts. Fifty-one patients with mitral annulus calcification and 27 controls had a stroke in the follow-up period. Mitral annulus calcification was not significantly associated with stroke in proportional hazards models (hazard ratio 0.76, 95% confidence interval 0.42-1.36, P = 0.3), or with any of the stroke subtypes, or with the presence of silent brain infarcts after adjustments for risk factors for generalized vascular disease Hypertension and carotid atheroma, with or without stenosis, ipsilateral or contralateral to the side of the stroke, were significantly associated with stroke in our patients. This study does not support the view that mitral annulus calcification is a risk factor for stroke. As others have found strong associations between mitral annulus calcification and cardiac and vascular risk factors for stroke, the increased risk of stroke in patients with mitral annulus calcification reported may be explained by these confounding risk factors. Therefore, in our opinion, mitral annulus calcification requires treatment of cardiovascular risk factors, but generally no specific measures such as surgery or oral anticoagulants are required to lower the risk of stroke.

Both cerebellar dysfunction and proprioceptive deficits have been described as the cause of the ataxia in patients with ataxic hemiparesis. In order to determine the cause of the ataxia, we investigated the sensory modalities and performed median nerve somatosensory evoked potentials (SEPs) in 19 patients with hemiataxia following lacunar ischaemic stroke. All patients had computer tomography (CT) and/or magnetic resonance imaging (MRI) of the brain. SEP results were reviewed for correlation with clinical features and infarct location and size. In all patients, eye closure did not worsen the ataxia. There was no difference between the mean latency of the SEP components from the affected and non-affected hemisphere of the brain in all patients. Only two of the 19 patients had abnormal SEPs. There was no correlation between SEP findings, clinical features and location or size of the infarcts. The discovery of normal SEPs in most cases and the clinical aspects of the ataxia suggest that hemiataxia following lacunar ischaemic stroke is usually of the cerebellar type and that disturbed proprioception is unlikely as the cause in most patients. Cerebellar-like ataxia is most likely caused by disruption of the cerebellar pathways at the level of the internal capsule or corona radiata, i.e. either the ascending dentatorubrothalamocortical or the descending corticopontocerebellar pathways.

From an ongoing stroke registry, including all patients with a first cerebral infarct, we studied 41 borderzone small deep infarcts: (SDIs) in comparison with 123 remaining SDIs. We noted vascular ris

The aim of this study was to describe the clinical experience in 184 consecutive stroke patients first‐ever treated with recombinant tissue plasminogen activator (rt‐PA) at a single Dutch centre, with special emphasis on results among the very old. Outcome parameters were the modified Rankin scale (mRs) at 3 months and symptomatic intracranial haemorrhage (SICH). Outcome was related to age. A total of 184 patients were treated of whom 45 were 80 years of age or older (24%). Sixty two (45%) of 139 patients

Balance deteriorates with age, and may eventually lead to falling accidents which may threaten independent living. As Taekwondo contains various highly dynamic movement patterns, taekwondo practice may sustain or improve balance. Therefore, in 24 middle-aged healthy volunteers (40-71 year) we investigated effects of age-adapted taekwondo training of one hour a week during one year on various balance parameters, such as: motor orientation ability (primary outcome measure), postural and static balance test, single leg stance, one leg hop test, and a questionnaire. Motor orientation ability significantly increased in favor of the antero-posterior direction with a difference of 0.62 degrees towards anterior compared to pre-training measurement, when participants corrected the tilted platform rather towards the posterior direction; female gender being an independent outcome predictor. On postural balance measurements sway path improved in all 19 participants, with a median of 9.3 mm/sec (range 0.71-45.86), and sway area in 15 participants with 4.2 mm²/sec (range 17.39-1.22). Static balance improved with an average of 5.34 seconds for the right leg, and with almost 4 seconds for the left. Median single leg stance duration increased in 17 participants with 5 seconds (range 1-16), and in 13 participants with 8 seconds (range 1-18). The average one leg hop test distance increased (not statistically significant) with 9.5 cm. The questionnaire reported a better ‘ability to maintain balance’ in sixteen. In conclusion, our data suggest that age-adapted Taekwondo training improves various aspects of balance control in healthy people over the age of forty.

Age-related cognitive decline is associated with increased risk of disability, dementia and death. Recent studies suggest improvement in cognitive speed, attention and executive functioning with physical activity. However, whether such improvements are activity specific is unclear. Therefore, we aimed to study the effect of one year age-adapted Taekwondo training on several cognitive functions, including reaction/ motor time, information processing speed, and working and executive memory, in 24 healthy volunteers over forty. Reaction and motor time decreased with 41.2 seconds and 18.4 seconds (p=0.004, p=0.015), respectively. Digit symbol coding task improved with a mean of 3.7 digits (p=0.017). Digit span, letter fluency, and trail making test task-completion-time all improved, but not statistically significant. The questionnaire reported “better” reaction time in 10 and “unchanged” in 9 of the nineteen study compliers. In conclusion, our data suggest that age-adapted Taekwondo training improves various aspects of cognitive function in people over 40, which may, therefore, offer a cheap, safe and enjoyable way to mitigate age-related cognitive decline.

Controversies exist concerning factors that contribute to the occurrence of epileptic seizures after stroke. Therefore, we studied prospectively the occurrence of seizures in 322 patients with a first-ever CT-confirmed symptomatic territorial brain infarct involving the cortex. We also studied potential risk factors for seizures, and gave special attention to cortical infarct location. Fifty-four patients developed post-stroke seizures. We distinguished between early- and late-onset seizures, occurring within two weeks following stroke-onset, or later than two weeks, respectively. We found that patients of 65 years or older with a cardioembolic brain infarct involving the middle temporal or post-central gyrus, had an almost eight times increased risk of early-onset seizures, whereas patients with a large brain infarct involving the supramarginal or superior temporal gyrus, had a five times increased risk of late-onset seizures. We conclude that risk factors and epileptogenic cortical areas for post brain infarct seizures can be identified, which however, differ between early- and late-onset seizures. These two seizure types may also differ in terms of seizure mechanism. Our findings may influence the decision on prophylactic treatment with antiepileptic drugs in stroke patients.

Objectives: To investigate whether the extent of white matter lesions (WMLs) and the number of small deep infarcts and territorial infarcts progress over time in patients with stroke and to test the hypothesis that WMLs are associated with small deep infarcts. Design: Computed tomographic follow-up study in a cohort of 107 patients with ischemic stroke (median follow-up, 3.0 years). Setting: Primary and referral care center. Patients: Sixty-three of 144 registered patients with a first-ever symptomatic lacunar stroke and 44 of 155 with a territorial stroke entered this study. Forty-seven (33%) of the nonparticipating patients with a lacunar stroke and 54 (35%) of those with a territorial stroke died, and 34 (24%) and 57 (37%), respectively, refused computed tomographic follow-up. Main Outcome Measures: The extent of the WMLs and the number of small deep and territorial infarcts on computed tomographic scans at study entry and at follow-up. Results: Progression of WMLs occurred in 26 patients (26%), and multivariate regression analysis showed that it was associated with symptomatic lacunar stroke at study entry (adjusted odds ratio [aOR], 5.0; 95% confidence interval [CI], 1.2-20.3), silent small deep infarcts at study entry (aOR, 6.0; 95% CI, 1.0-34.6), old age (aOR, 5.5; 95% CI, 1.3-23.1), and longer follow-up (aOR, 12.7; 95% CI, 1.8-89.0). We found progression of small deep infarcts in 41 patients (38%). The progression was associated with symptomatic lacunar stroke at study entry (aOR, 27.7; 95% CI, 6.3-120.9) and longer follow-up (aOR, 7.7; 95% CI, 1.4-41.3). Progression of both WMLs and small deep infarcts, which occurred in 16 patients (16%), was associated with symptomatic lacunar stroke at study entry (aOR, 34.1; 95% CI, 2.5-471.7), silent small deep infarcts at study entry (aOR, 12.5; 95% CI, 1.4-112.0), and longer follow-up (aOR, 29.7; 95% CI, 1.8-501.0). The number of territorial infarcts increased in 14 patients (13%). The increase was associated with symptomatic territorial stroke at study entry (aOR, 7.9; 95% CI, 1.5-40.8) and a history of ischemic heart disease (aOR, 6.6; 95% CI, 1.3-34.8). Conclusions: The marked progression of WMLs and small deep infarcts that occurred mainly in patients with lacunar stroke suggests that both WMLs and small deep (lacunar) infarcts are caused by a similar vasculopathy that affects small vessels, which is progressive despite standard stroke treatment.

Although borderzone brain infarcts lack a uniform definition and are difficult to define because of significant variability in cerebral vascular supply, they are presumed to be related to haemodynamic

We studied the relationship between infarct size and degree of internal carotid artery stenosis in 227 stroke patients without a source of embolism in the heart, who had a CT-verified territorial brain infarct. We used logistic regression analysis adjusting for differences between groups in co-associated variables such as age, sex, hypertension, diabetes mellitus, and a history of ischaemic heart disease. Ipsilateral carotid stenosis greater than 50% was more strongly associated with large than small infarcts; adjusted odds ration [(a)OR]: 4.56; 95% confidence interval (CI): 1.21-17.2; P = 0.02. For ipsilateral carotid occlusion the association was even stronger--(a)OR: 36.80; 95% CI: 2.54-533; P = 0.007. When large infarcts were compared with infarcts of small and moderate size together the ORs were 2.29, 95% CI 1.14-4.58 and 2.57, 95% CI 1.17-5.67 for carotid stenosis or occlusion, respectively. Our data show a relationship between greater than 50% carotid stenosis or occlusion and large brain infarcts. We suggest that haemodynamic impairment may contribute to infarct size in territorial infarcts of non-cardiac origin.

The difference in stroke causes between younger and elderly stroke patients may largely depend on differences in the cause of cortical ischaemic stroke, the pathogenesis in lacunar ischaemic stroke be

We wanted to establish independent associations of various clinical variables, computed tomographic (CT) scan features, presenting stroke subtypes, and outcome with the presence of silent infarcts on CT. We studied 755 consecutive patients in a prospective registration of patients with first-ever supratentorial atherothrombotic, cardioembolic, or lacunar stroke or stroke of undetermined cause by multiple logistic regression analysis. Two hundred six patients (27%) with a first symptomatic territorial or small deep ischemic stroke had one or more silent infarcts on CT. Of all silent lesions, 169 (82%) were small and deep. Silent infarcts were significantly more strongly associated with a lacunar than atherothrombotic (odds ratio [OR], 1.59; 95% confidence interval [CI], 1.02 to 2.47; P = .039) or cardioembolic (OR, 1.89; 95% CI, 1.2 to 2.99; P = .005) index stroke. Silent territorial lesions were more strongly associated with cardioembolic than with lacunar stroke but not with atherothrombotic stroke. In this respect, no differences were found between the atherothrombotic and undetermined-cause group. Advanced age and hypertension were the only risk factors that were significantly associated with silent infarcts (OR, 1.76; 95% CI, 1.14 to 2.71; P = .011; and OR, 1.58; 95% CI, 1.13 to 2.21; P = .007; respectively), mainly because of a strong independent association of these risk factors with silent small deep infarcts (OR, 1.75; 95% CI, 1.10 to 2.79; P = .018; and OR, 1.57; 95% CI, 1.09 to 2.24; P = .014; respectively). A cardioembolic source or atrial fibrillation in specific was not independently associated with any type or number of silent infarcts. Significant carotid stenosis (diameter reduction > 50%) was not significantly associated with any type of silent lesion. Initial severe handicap (Rankin Scale score > 3), 30-day case fatality rate, and 1-year mortality were not affected by the presence of silent infarcts. The strong association of silent small deep lesions with first symptomatic small deep infarcts suggests a common underlying mechanism (presumably small-vessel vasculopathy), whereas cardiogenic embolism and large-vessel thromboembolism are the most likely causes in both silent and first symptomatic territorial infarcts. Single or multiple silent infarcts do not predict a cardioembolic stroke mechanism in first symptomatic supratentorial brain infarcts. As silent infarcts do not predict the cause of carotid embolic stroke in first symptomatic brain infarcts, their presence should not influence the decision on carotid surgery. Silent infarcts do not affect the degree of initial handicap, 30-day case fatality, or 1-year mortality. The significance of silent infarcts for predicting possible future cognitive decline and risk of recurrent stroke deserves further study.

Our goal was to identify factors that play a role in false clinical diagnosis of small deep infarcts. In 350 prospectively registered patients with a first supratentorial ischemic stroke, we clinically differentiated between lacunar and nonlacunar syndromes. Using computed tomography (CT), we distinguished small deep and territorial infarcts and also recorded leukoaraiosis and asymptomatic infarcts. Degree of initial handicap, potential source of cardioembolic stroke, and hypertension were also noted. One hundred forty-seven patients had a lacunar and 203 a nonlacunar syndrome. Forty-two (12%) had a lesion visualized by CT that was compatible with a recent infarct but was considered inappropriate for the clinical syndrome: nineteen had a nonlacunar syndrome but a small deep infarct, and 23 had a lacunar syndrome but a territorial infarct. Patients with a nonlacunar syndrome but a small deep infarct were more severely disabled (a modified Rankin scale rating of 5) (odds ratio [OR], 4.31; 95% confidence interval [CI], 1.25 to 14.88) and had a cardioembolic source (OR, 4.07; 95% CI, 1.04 to 15.95), leukoaraiosis (OR, 3.79; 95% CI, 1.32 to 10.05), or asymptomatic infarcts visualized by CT (OR, 4.13; 95% CI, 1.45 to 11.71) compared with 124 patients with a correctly diagnosed small deep infarct. Twelve of 19 patients with a nonlacunar syndrome but a small deep infarct had a lesion in the left hemisphere, and 9 of these 12 had "aphasia." Patients with a lacunar syndrome but a territorial infarct more often had a cardioembolic source (OR, 4.02; 95% CI, 1.15 to 14.03) and a pure motor syndrome (OR, 4.52; 95% CI, 1.55 to 13.18) than those with lacunar syndrome but a small deep infarct, although 21 (91%) were in the right hemisphere. Of the first 103 patients with lacunar stroke diagnosed by two of the study neurologists, 5 had an inappropriate lesion compared with 14 of the later 40 diagnosed by colleagues without a specific interest in cerebrovascular diseases (OR, 0.09; 95% CI, 0.03 to 0.26). (1) Diagnosis of lacunar syndromes should not be influenced by deficit severity or the presence of a potential cardiac source of embolism. (2) Speech disorders should carefully be classified. (3) Routine tests of nondominant higher functions may be inadequate. (4) Doctors interested in cerebrovascular neurology have a lower failure rate in differentiating small deep infarcts from territorial infarcts than those less well-trained or interested in neurology. (5) Among the lacunar syndromes, pure motor syndrome may be the least specific predictor of a small deep infarct.