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D Leys

Publications and source records attributed to D Leys.

At least 73 records · Page 4Linked to original sources
PubMed2001

A new rating scale for age-related white matter changes applicable to MRI and CT.

BACKGROUND AND PURPOSE: MRI is more sensitive than CT for detection of age-related white matter changes (ARWMC). Most rating scales estimate the degree and distribution of ARWMC either on CT or on MRI, and they differ in many aspects. This makes it difficult to compare CT and MRI studies. To be able to study the evolution and possible effect of drug treatment on ARWMC in large patient samples, it is necessary to have a rating scale constructed for both MRI and CT. We have developed and evaluated a new scale and studied ARWMC in a large number of patients examined with both MRI and CT. METHODS: Seventy-seven patients with ARWMC on either CT or MRI were recruited and a complementary examination (MRI or CT) performed. The patients came from 4 centers in Europe, and the scans were rated by 4 raters on 1 occasion with the new ARWMC rating scale. The interrater reliability was evaluated by using kappa statistics. The degree and distribution of ARWMC in CT and MRI scans were compared in different brain areas. RESULTS: Interrater reliability was good for MRI (kappa=0.67) and moderate for CT (kappa=0.48). MRI was superior in detection of small ARWMC, whereas larger lesions were detected equally well with both CT and MRI. In the parieto-occipital and infratentorial areas, MRI detected significantly more ARWMC than did CT. In the frontal area and basal ganglia, no differences between modalities were found. When a fluid-attenuated inversion recovery sequence was used, MRI detected significantly more lesions than CT in frontal and parieto-occipital areas. No differences were found in basal ganglia and infratentorial areas. CONCLUSIONS: We present a new ARWMC scale applicable to both CT and MRI that has almost equal sensitivity, except for certain regions. The interrater reliability was slightly better for MRI, as was the detectability of small lesions.

Aging↗
PubMed2001

Atherothrombosis--the neurologist's point of view.

Patients with peripheral arterial disease (PAD) have an increased risk of cerebral ischaemia, but many transient ischaemic attacks are not recognized by patients, or by physicians who are not neurologists. Similarly, PAD is common in stroke patients, but often remains unrecognized by neurologists. Major long-term risks in patients with cerebral ischaemia due to atherosclerosis are myocardial infarction and recurrence of stroke. Neurologists should consider concomitant PAD when choosing a treatment strategy. Patients with PAD need to be educated about their risk for cerebral ischaemic events, and physicians caring for PAD patients need to identify those individuals who may require carotid surgery. The appropriate strategy for prevention of stroke in PAD patients consists of optimal management of risk factors for stroke (smoking, arterial hypertension, hypercholesterolaemia), antiplatelet therapy with clopidogrel as first-choice treatment, and carotid surgery in patients with high-grade stenosis of the internal carotid artery who are at low risk for surgery.

Clopidogrel↗
PubMed2001

[Vascular dementia].

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Cross-Sectional Studies↗
PubMed2000

[Cerebral amyloid angiopathies].

PATHOLOGY FINDINGS: Cerebral amyloid angiopathies are defined by the presence of amyloid deposits on the walls of cerebral vessels. These amyloid deposits are found in the media of arterioles of the leptomeninges and the cortex. They are sometimes associated with Alzheimer-type lesions. Overt amyloid vasculopathy characterized by lesions of the vascular wall with a media totally replaced by amyloid substance may be observed. CLINICAL EXPRESSION: Lobular hemorrhage, often with recurrent episodes is the most frequent manifestation of cerebral amyloid angiopathy. Cerebral infarcts or leukoencephalopathy may also be observed. An association with cerebral angiitis has been reported in a few cases. SPORADIC OR FAMILIAL DISEASE: Several types can be distinguished depending on the sporadic or familiar nature of the disease pattern as well as the chemical make-up of the protein deposit. In sporadic cerebral amyloid angiopathy the deposit is composed of protein A beta, and in familial cases, of protein A beta, cystatin C, gelsosine or transthyretin. Mutation of the genes coding for amyloid substance constituents have been identified in diverse forms of familial cerebral amyloid angiopathy.

Adult↗
PubMed2000

Crystal structures of an oxygen-binding cytochrome c from Rhodobacter sphaeroides.

The photosynthetic bacterium Rhodobacter sphaeroides produces a heme protein (SHP), which is an unusual c-type cytochrome capable of transiently binding oxygen during autooxidation. Similar proteins have not only been observed in other photosynthetic bacteria but also in the obligate methylotroph Methylophilus methylotrophus and the metal reducing bacterium Shewanella putrefaciens. A three-dimensional structure of SHP was derived using the multiple isomorphous replacement phasing method. Besides a model for the oxidized state (to 1.82 A resolution), models for the reduced state (2.1 A resolution), the oxidized molecule liganded with cyanide (1. 90 A resolution), and the reduced molecule liganded with nitric oxide (2.20 A resolution) could be derived. The SHP structure represents a new variation of the class I cytochrome c fold. The oxidized state reveals a novel sixth heme ligand, Asn(88), which moves away from the iron upon reduction or when small molecules bind. The distal side of the heme has a striking resemblance to other heme proteins that bind gaseous compounds. In SHP the liberated amide group of Asn(88) stabilizes solvent-shielded ligands through a hydrogen bond.

Bacterial Proteins↗
PubMed2000

The anatomy of aphasia revisited.

OBJECTIVE: To determine lesion locations associated with the various types of aphasic disorders in patients with stroke. BACKGROUND: The anatomy of aphasia has been challenged by several recent studies. Discrepancies are likely to be due to methodologic issues. METHODS: We examined 107 patients with a standardized aphasia battery and MRI. Three examiners blinded to the clinical data rated signal abnormalities in 69 predetermined regions of interest. The statistical procedure used classification tree testing, which selected regions associated with each aphasic disorder. RESULTS: 1) Nonfluent aphasia depended on the presence of frontal or putaminal lesions; 2) repetition disorder on insula-external capsule lesions; 3) comprehension disorder on posterior lesions of the temporal gyri; 4) phonemic paraphasia on external capsule lesions extending either to the posterior part of the temporal lobe or to the internal capsule; 5) verbal paraphasia on temporal or caudate lesions; and 6) perseveration on caudate lesions. These analyses correctly classified 67% to 94% of patients. CONCLUSIONS: Lesion location is the main determinant of aphasic disorders at the acute stage. Most clinical-radiologic correlations supported the classic anatomy of aphasia.

Adolescent↗
PubMed2000

Thalamic tremor: correlations with three-dimensional magnetic resonance imaging data and pathophysiological mechanisms.

Tremor associated with a single focal thalamic lesion has rarely been reported. Furthermore, the exact localization of the lesions is difficult to determine because of the imprecision of "conventional" radiology (computed tomography scan and/or "standard" magnetic resonance imaging). The aim of this study was to identify which thalamic structures are involved in tremor associated with a single focal thalamic lesion. We selected two patients who presented with unilateral postural and kinetic tremor of the upper limb related to a localized thalamic infarction. Three-dimensional T1-weighted magnetic resonance imaging sequence (MP-RAGE sequence) was used to determine the precise topography of the lesions by stereotactic analysis using the atlas of Hassler. The lesions were located within the pulvinar, the sensory nuclei, the mediodorsal nucleus, and the ventral lateral posterior nucleus (according to the classification of Hirai and Jones), the latter including the ventral intermediate nucleus (Vim according to the classification of Hassler). However, the Vim was spared. The subthalamic area, which can induce tremor, was not involved. After having compared the topography of the lesions with the clinical findings, we suggest that thalamic tremors may result from the interruption of the cerebellar outflow tract to the Vim within the thalamus.

Adult↗
PubMed2000

How can cerebral infarcts and hemorrhages lead to dementia?

The incidence of new onset dementias is increased after stroke. The objective of this review is to investigate how cerebral infarcts and hemorrhages can lead to dementia. Stroke subtypes, total volume of cerebral lesion and functional tissue loss, and location of the lesions are the major determinant of dementia in stroke patients. The causal relationship between stroke and dementia is clear: (1) in young patients who are unlikely to have associated Alzheimer pathology; (2) when the cognitive functioning was normal before stroke, impaired immediately after, and does not worsen over time; (3) when the lesions are located in strategic areas; and (4) when a well-defined vasculopathy known to be associated with dementia is proven. However, white matter changes and associated Alzheimer pathology may also contribute to the dementia syndrome in stroke patients.

Brain↗
PubMed2000

Long-term evaluation of autonomic tone in patients below 50 years of age with unexplained cerebral infarction: relation to atrial vulnerability.

UNLABELLED: Preliminary studies have described, in young patients with unexplained cerebral infarction, electrophysiological abnormalities similar to those observed in paroxysmal atrial fibrillation. Moreover, in young adults with 'normal' hearts, increased susceptibility to paroxysmal atrial fibrillation with autonomic abnormalities as assessed by heart rate variability analysis have been reported. METHODS: The long-term time and frequency domain measures of heart rate variability were analysed prospectively from 24-h Holter ECG recordings in 25 patients (39 +/- 8 years) with unexplained cerebral infarction, and in 25 age-, sex- and cigarette-smoking-matched healthy control subjects. The day following the Holter ECG recordings, 9 +/- 4 months (mean) after the stroke, stroke patients underwent an electrophysiological study in order to analyse the electrical characteristics of their right atria and also to determine their vulnerability to atrial fibrillation. The correlations between autonomic tone parameters and electrophysiological findings were therefore assessed with linear regression analyses. RESULTS: All the measured components of heart rate variability either in time (SDNN, pNN50, SDANN/5, rMSSD) or frequency domains (total power, low-frequency, high-frequency power, low-frequency/high-frequency power ratio) were similar between stroke patients and controls. During electrophysiological study, atrial fibrillation was induced in 80% of stroke patients. Among these patients, atrial refractory periods were significantly shorter, local electrograms were longer, and latent atrial vulnerability index was markedly decreased when compared with patients having no inducible atrial fibrillation. Concerning heart rate variability analysis, no difference was found between patients with induced atrial fibrillation when compared with a matched subgroup of healthy control subjects. Furthermore, there was no statistically linear correlation between any of the measured autonomic tone parameters and any of the discovered atrial vulnerability markers. CONCLUSIONS: The long-term autonomic tone parameters of young patients presenting with a history of unexplained cerebral infarction are similar to those of healthy control subjects and are not correlated with atrial vulnerability parameters or atrial fibrillation inducibility.

Adult↗
PubMed2000

Increase in endogenous brain superoxide dismutase as a potential mechanism of lipopolysaccharide-induced brain ischemic tolerance.

A low dose (0.5 mg/kg) of lipopolysaccharide (LPS), administered 72 hours before 60-minute middle cerebral artery occlusion, induced a delayed neuroprotection proven by the significant decrease (-35%) of brain infarct volume in comparison with control, whereas infarct volumes remained unchanged in rats treated 12, 24, or 168 hours before ischemia. This delayed neuroprotective effect of LPS was induced only with low doses (0.25 to 1 mg/kg), whereas this effect disappeared with a higher dose (2 mg/kg). The delayed neuroprotection of LPS was induced in the cortical part of the infarcted zone, not in the subcortical part. The beneficial effect of LPS on consequences of middle cerebral artery occlusion was suppressed by dexamethasone (3 mg/kg) and indomethacin (3 mg/ kg) administered 1 hour before LPS, whereas both drugs had no direct effect on infarct volume by themselves, suggesting that activation of inflammatory pathway is involved in the development of LPS-induced brain ischemic tolerance. Preadministration of cycloheximide, an inhibitor of protein synthesis, also blocked LPS-induced brain ischemic tolerance suggesting that a protein synthesis is also necessary as a mediating mechanism. Superoxide dismutase (SOD) could be one of the synthesized proteins because lipopolysaccharide increased SOD brain activity 72 hours, but not 12 hours, after its administration, which paralleled the development of brain ischemic tolerance. In contrast, catalase brain activity remained unchanged after LPS administration. The LPS-induced delayed increase in SOD brain content was suppressed by a previous administration of indomethacin. These data suggest that the delayed neuroprotective effect of low doses of LPS is mediated by an increased synthesis of brain SOD that could be triggered by activation of inflammatory pathway.

Adaptation, Physiological↗
PubMed2000

Relevance of white matter changes to pre- and poststroke dementia.

White matter changes are often associated with stroke, risk factors for stroke, and dementia. From a theoretical point of view, they may be associated with an increased risk of pre- or poststroke dementia because (i) they are linked with subtle cognitive decline, which may add to the consequences of the stroke lesions and of associated Alzheimer pathology; and (ii) they indicate an increased risk of stroke recurrence. The aim of this study was to evaluate the contribution of white matter changes to pre- and poststroke dementia. The relationship between preexisting dementia and white matter changes was evaluated in the Lille stroke-dementia cohort. We assessed the cognitive functioning prior to stroke in 202 consecutive patients with ischemic or hemorrhagic stroke, by means of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). We classified in the dementia group patients with IQCODE scores of 104 or more. White matter changes were rated on CT with the Blennow's rating scale. Thirty-three of 202 patients were demented before stroke (16.3%; 95% confidence interval: 11.2-21.4); the logistic regression analysis found that female sex, family dementia, white matter changes, and cerebral atrophy were independently associated with prestroke dementia. White matter changes were also associated with an increased risk of poststroke dementia, 2 years after stroke onset. Thus, white matter changes contribute to dementia occurring in stroke patients.

Adult↗