Jan Lodder - Academia.edu (original) (raw)

Papers by Jan Lodder

European Journal of Neurology, 1997

ABSTRACT

Journal of the Neurological Sciences, 2002

This study investigated the occurrence of cognitive disorders 1 and 6 months after stroke in a co... more 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, agez40, 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.

BMJ, 1988

The benefits of long term anticoagulant treatment of patients with non-rheumatic atrial fibrillat... more The benefits of long term anticoagulant treatment of patients with non-rheumatic atrial fibrillation and cerebral infarction were studied by comparing two series of patients with stroke from centres with different policies on anticoagulant treatment. The long term prognosis of 50 patients from the Oxfordshire community stroke project, who did not receive anticoagulants, was compared with that of 70 similar patients from Maastricht, who were treated with anticoagulants. After a mean foliow up of 27 months there was no significant difference in either the rate of survival or the rate of recurrent stroke between the two groups. These data suggest that any benefit of anticoagulation is modest. A large randomised trial is planned to establish whether long term anticoagulant treatment is of value and, if so, to what extent.

Stroke, 1994

We would like to thank Dr Alpert for his comment on our article, in which we demonstrated that ex... more We would like to thank Dr Alpert for his comment on our article, in which we demonstrated that extracranial carotid atherosclerosis is increasing in Japanese patients with brain ischemia. 1 We also reviewed some vascular risk factors possibly related to our findings; these include hypertension, diabetes mellitus, ischemic heart disease, and hypercholesterolemia. This list of risk factors is rather incomplete because of the failure to obtain thorough medical histories from the early patients (1963 to 1965). We are aware that some important risk factors, including smoking, are missing from our analysis, and hence we do not conclude that diabetes mellitus is the only risk factor responsible for the change in the rate of extracranial cerebral atherosclerosis in the Japanese population. Accordingly, we respect the comment made by Dr Alpert, and do not exclude the possibility that smoking played an important role in the increase in extracranial carotid atherosclerosis revealed by our analysis.

Background Using Surface-Enhanced Laser Desorption/Ionization Time-of-Flight Mass Spectrometry, w... more Background Using Surface-Enhanced Laser Desorption/Ionization Time-of-Flight Mass Spectrometry, we aimed to detect differences in protein expression profile in serum samples of two lacunar stroke subtypes. Methods Surface-Enhanced Laser Desorption/Ionization Time-of-Flight Mass Spectrometry, followed by protein identification, was performed in samples of eight first-ever lacunar stroke patients with MR imaging showing a single symptomatic lacunar lesion (type I), and eight with multiple additional "silent" lacunar lesions and extensive white matter lesions (type II). Results A 16 kDa protein, identified as alpha-2-chain of haptoglobin (Hp), was up-regulated in type I compared to type II (peak intensity 12.5 vs. 5.0; p=0.02). A polymorphism with two alleles, Hp-1 and Hp-2, determines the presence of alpha-1 and/or alpha-2-chains in the Hp-molecule. Therefore, Hp phenotypic analysis was performed. Hp-1 : Hp-2 allele frequency was 0.562 : 0.438 in type I and 0.812 : 0.188 in type II (population reference ~0.4 : 0.6). Conclusions The up-regulation of the alpha-2-chain in type I is (partly) related to a higher Hp-2 allele frequency. Yet, compared to population reference, the phenotype distribution in both lacunar stroke patient groups deviates towards a high Hp-1 allele frequency, suggesting a role for the Hp gene in the etiology of cerebral small vessel disease. The even higher Hp-1 allele frequency in type II than in type I implies a promoting role for Hp-1 in developing multiple silent lacunar lesions and white matter lesions and could be a reflection of a difference in underlying vascular pathology between the two types, but needs confirmation in larger series.

Current Neurovascular Research, 2008

Stroke, 2011

Background and Purpose— Cerebral small vessel disease (CSVD) may be caused by endothelial dysfunc... more 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±interqua...

Journal of Neurology, 1996

Clinical Neurology and Neurosurgery, 1987

Cerebrovascular Diseases, 1996

Cerebrovascular Diseases, 1997

ABSTRACT In many young stroke patients the cause of stroke remains unclear. Enhanced red blood ce... more ABSTRACT In many young stroke patients the cause of stroke remains unclear. Enhanced red blood cell aggregation is considered a factor related to the pathogenesis of stroke in elderly patients, in whom enhanced red blood cell aggregation is correlated with increased fibrinogen. We determined red blood cell aggregation, fibrinogen concentration, hematocrit value and erythrocyte sedimentation rate in 18 stroke patients ≤ 50 years of age in the early phase and in 40 stroke patients ≤ 50 years in the late phase, and compared the values with those in young control persons. We also determined these variables in stroke patients ≤ 60 years of age in the early and in the late phases and in elderly controls. In young stroke patients we found an enhanced red blood cell aggregation compared with young controls (p < 0.00005), both in the early and in the late phases, whereas fibrinogen was normal. Red blood cell aggregation was significantly associated with stroke after adjusting for fibrinogen, hematocrit and erythrocyte sedimentation rate [adjusted odds ratio 16.20; 95% confidence interval (CI) 2.80–93.61]. Red blood cell aggregation was higher in elderly patients than in elderly controls (p < 0.05). In elderly patients fibrinogen was associated with stroke (crude odds ratio 12.92; 95% CI 2.54–65.82), whereas after adjusting for red blood cell aggregation, fibrinogen, hematocrit and erythrocyte sedimentation rate only erythrocyte sedimentation rate showed a significant association with stroke (odds ratio 26.37; 95% CI 1.93–359.74). In conclusion, enhanced red blood cell aggregation independently relates to stroke in young people, which may suggest that enhanced red blood cell aggregation contributes to stroke cause, whereas in elderly patients any such effect is probably related to confounding by raised fibrinogen.

Neurobiology of aging, 2012

Cerebral small vessel disease (CSVD) is considered to be caused by an increased permeability of t... more Cerebral small vessel disease (CSVD) is considered to be caused by an increased permeability of the blood-brain barrier and results in enlargement of Virchow Robin spaces (VRs), white matter lesions, brain microbleeds, and lacunar infarcts. The increased permeability of the blood-brain barrier may relate to endothelial cell activation and activated monocytes/macrophages. Therefore, we hypothesized that plasma markers of endothelial activation (adhesion molecules) and monocyte/macrophage activation (neopterin) relate to CSVD manifestations. In 163 first-ever lacunar stroke patients and 183 essential hypertensive patients, we assessed CSVD manifestations on brain magnetic resonance imaging (MRI) and levels of C-reactive protein (CRP), neopterin, as well as circulating soluble adhesion molecules (sICAM-1, sVCAM-1, sE-selectin, sP-selectin). Neopterin, sICAM-1 and sVCAM-1 levels were higher in patients with extensive CSVD manifestations than in those without (p < 0.01). Neopterin lev...

Journal of Hypertension, 2000

Background and Purpose— Results from case-control and case-case studies indicate that a positive ... more 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 (<65 years) probands, ...

BACKGROUND AND PURPOSE Blood-brain barrier dysfunction may be an early phenomenon in the developm... more 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 m...