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Biomedical subjects

D Leys

Publications and source records attributed to D Leys.

At least 145 records · Page 8Linked to original sources
PubMed1995

Systemic vascular smooth muscle cell impairment in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is characterized by a cerebral non-atherosclerotic, nonamyloid angiopathy mainly affecting the small arteries penetrating the white matter. In the brain vessels of two patients with CADASIL, abnormal patches of granular osmiophilic material have recently been described. Here we report the observation of similar granular osmiophilic material within the vessel walls of muscle and skin biopsies from a 54-year-old woman belonging to a CADASIL family, who suffered from subcortical dementia with leukoencephalopathy demonstrated on neuroimaging. Postmortem examination disclosed changes of the vessel walls in all the organs chiefly leading to cerebral lesions. Ultrastructural study showed destruction of the vascular smooth muscle cells (VSMC) and the granular osmiophilic material already found in muscle and skin biopsies in this patient. Both changes were found all along the arterial tree. The findings of this study indicate that CADASIL is a systemic vascular disease involving arterial VSMC and that the lesions are different in each organ and vessel wall, depending on their fine structure. Moreover, it emphasizes that skin and muscle biopsies might be useful for diagnosis of and research into CADASIL.

Brain↗
PubMed1995

Small subcortical infarcts and primary subcortical haemorrhages may have different risk factors.

Primary subcortical haemorrhages (SCH) and small subcortical infarcts (SSI) arise from changes in penetrating perforating arteries. The aim of this study was to compare cerebrovascular risk factors between patients with SCH and patients with SSI. Of 396 patients with a first-ever stroke (226 males; 170 females; median-age: 63), 108 had SSI, and 64 SCH, with or without subcortical infarcts co-existing. Patients with SCH were less likely to have current atrial fibrillation or associated non-lacunar infarcts, but they were more likely to have arterial hypertension (except after exclusion of patients with co-existence of SSI and SCH) and alcoholism, and they were significantly younger and had lower leukoaraiosis scores. The independent factors for SCH were alcoholism, arterial hypertension and lack of significant internal carotid artery stenosis. The only independent factor for SSI was leukoaraiosis score. Hypertension was the most important risk factor in both groups, but its prevalence was higher in the SCH group. Whether patients will develop SSI or SCH probably depends on associated risk factors such as alcohol consumption. Further studies should also take into account the characteristics of arterial hypertension.

Adult↗
PubMed1995

[Neurologic manifestations associated with antiphospholipid antibodies. Or what remains of neurolupus?].

Antiphospholipid antibody is associated with a clinical syndrome of vascular thrombosis, thrombocytopenia, recurrent fetal loss and livedo reticularis, whether or not a clinical diagnosis of systemic lupus erythematosus (SLE) coexists. Central nervous system involvement in SLE is multifactorial, thrombotic events, antineuronal antibodies, hypertension, infection, side effects of drugs etc. Antiphospholipid antibodies may play a role in focal neurological manifestations in SLE. In the absence of SLE, different neurological symptoms are well associated with antiphospholipid antibodies including stroke, seizures, dementia, migraine, ocular ischemia, chorea, transverse myelopathy, cerebral phlebitis. Other association are more controversal like Guillain Barré syndrome, motor neuron disease, communicating hydrocephalus. In all patients with antiphospholipid antibodies with neurological involvement, cerebral MRI may be performed with an echocardiographic study because a possible association with Libman and Sacks endocarditis, valve dysfunction or cardiac thrombus source of cerebral ischemia.

Antibodies, Antiphospholipid↗
PubMed1995

[Morphological imaging in the diagnosis of dementia. II. Vascular dementia].

Magnetic resonance imaging (MRI) and CT-scan are crucial for the diagnosis of cerebrovascular diseases. Multi-infarct dementias may be divided into (i) dementias due to multiple cortical infarcts and (ii) dementias due to multiple lacunar infarcts in the basal ganglia, thalamus and hemispheric white matter, usually associated with leukoaraiosis. A single infarct located in the thalamus or in the left angular gyrus may also induce dementia. Abnormalities of the cerebral white matter, so-called leukoaraiosis, are usually the consequence of a cerebrovascular disease and may be called Binswanger's disease in severe cases. However, leukoaraiosis is not specific of vascular dementia and may also be found in Alzheimer's disease and even in normal aging.

Brain↗
PubMed1995

Psychoacoustical deficits related to bilateral subcortical hemorrhages. A case with apperceptive auditory agnosia.

We report a case of acute deafness secondary to bilateral hemorrhages involving the external capsule and extending to both temporal isthmi. The lesions probably disrupted both auditory radiations. Deafness disappeared within 2 weeks leading to a transient auditory agnosia for environmental and verbal sounds. Performance on audiological and neurolinguistic tests were consistent with the hypothesis of a deficit of non-specific auditory processes. Psychoacoustical deficits related to subcortical lesions are very rare and might differ from those due to cortical lesions by the lack of aphasia. The present case and both previous cases with subcortical lesions might suffer from auditory agnosia of apperceptive type. Its characteristics and the role of non-specific auditory processes are discussed using the data obtained from this third case.

Agnosia↗
PubMed1995

Cerebellar border zone infarcts are often associated with presumed cardiac sources of ischaemic stroke.

It has been suggested that most border zone cerebellar infarcts are embolic infarcts or infarcts due to hypercoagulatble states. The aim of this study was to test this hypothesis. Risk factors for the presumed mechanism of stroke (TOAST criteria) were studied in 14 consecutive patients (nine men, five women; age range 29-84 years) with a total of 17 border zone cerebellar infarcts. The presumed cause of stroke was "cardioembolism" in nine patients. Three patients had a dissection of the vertebral artery. Two patients had a negative diagnostic investigation, and one had a cardiac arrest. These findings support the hypothesis that cardioembolism is a frequent mechanism of border zone cerebellar infarcts.

Adult↗
PubMed1995

Postpartum cerebral angiopathy possibly due to bromocriptine therapy.

BACKGROUND: Eight cases of benign angiopathy of the postpartum period have been reported previously, none of which involved the administration of bromocriptine. CASE DESCRIPTION: We describe a case of benign cerebral angiopathy in a 20-year-old woman in the postpartum period occurring after bromocriptine therapy prescribed to suppress lactation. CONCLUSIONS: Other adverse effects due to vasoconstriction have been reported during bromocriptine therapy, such as myocardial infarction and arterial hypertension. This case suggests that a similar mechanism may be possible in cerebral arteries, although the cause of vasoconstriction remains uncertain.

Adult↗
PubMed1995

Early predictors of death and disability after acute cerebral ischemic event.

BACKGROUND AND PURPOSE: Many clinical trials are currently being conducted to evaluate the ability of neuroprotectors and thrombolytic agents to improve survival and functional outcome after ischemic stroke. Such trials require early predictors of survival and disability for ethical and methodological reasons. The aim of the study was to determine which variables, of those easily assessable during the first 24 hours after stroke onset, would be predictors of 8-day mortality rate and 3-month clinical outcome. METHODS: One hundred fifty-two consecutive patients with an acute ischemic event were evaluated within 24 hours after symptom onset. We determined (1) the 8-day mortality rate and (2) the 3-month functional outcome (Glasgow Outcome Scale). The following potential predictors of outcome were tested by means of a stepwise logistic regression analysis: age, sex, body mass index, atrial fibrillation, previous stroke, existence of headache, Orgogozo score, level of consciousness, swallowing disturbances, hemianopia, pulse rate, mean blood pressure, hematocrit, glycemia, and computed tomographic scan data (cerebral atrophy score, hyperdense middle cerebral artery sign, number of silent infarcts, leukoaraiosis score). RESULTS: The multivariate analysis revealed that the 8-day mortality rate depended only on the level of consciousness at admission (P = .0001); death or dependence at month 3 (scores 3 to 5 on the Glasgow Outcome Scale) depended on the severity of the clinical deficits (P = .0001), previous stroke (P = .0018), and age (P = .0237). CONCLUSIONS: In future drug trials, the distribution of patients between "active treatment" and "placebo" groups should be balanced regarding the severity of clinical deficits, history of stroke, and age.

Acute Disease↗
PubMed1995

Stroke patterns in unilateral atherothrombotic occlusion of the internal carotid artery.

BACKGROUND AND PURPOSE: Stroke patterns in patients with occlusion of the internal carotid artery (ICA) and no potential cardiac cause of stroke remain unknown. The aim of our study was to determine the pattern of stroke in patients with an occlusion of the ICA of presumed atherosclerotic origin. METHODS: Of 873 consecutive patients admitted for an acute ischemic event during a 49-month period, 40 (29 men and 11 women; mean age, 63 years) had a unilateral occlusion of the ICA of presumed atherosclerotic origin and no other potential cause of stroke. They underwent two computed tomographic scans, Doppler ultrasonography, and B-mode echotomography of the cervical arteries or angiography and echocardiography. We compared stroke patterns between both hemispheres. RESULTS: We found ipsilateral infarcts in 32 patients (80%; 99% confidence interval [CI], 64% to 96%) and contralateral infarcts in 12 patients (30%; 99% CI, 11% to 49%). Infarcts ipsilateral to the ICA occlusion were more likely to be cortical (odds ratio, 9.33; 99% CI, 2.4 to 36.35) or subcortical infarcts 15 mm or greater (odds ratio, 16.71; 99% CI, 1.05 to 267.3). The prevalence of subcortical infarcts less than 15 mm did not differ between hemispheres. CONCLUSIONS: Symptomatic infarcts related to an ICA occlusion are more likely to be cortical or large subcortical infarcts. Small subcortical infarcts have the same prevalence in both hemispheres and therefore may be coincidental.

Acute Disease↗
PubMed1995

Computed tomographic angiography for the evaluation of carotid artery stenosis.

BACKGROUND AND PURPOSE: No previous study has compared the reliability of carotid artery measurement provided by axial images, shaded surface display (SSD), and maximum intensity projection (MIP). METHODS: Helical CT and conventional angiography were performed prospectively in 20 patients with atherosclerotic stenosis of the internal carotid artery. Stenosis measurement was performed in a blinded fashion on angiography and CT by two independent examiners. Calcifications were segmented when they were located far enough from the vascular lumen. SSD and MIP were systematically performed for each carotid bifurcation. We measured stenosis using conventional angiography as standard and the different CT reconstructions (axial images, SSD, and MIP) by comparing the stenosis diameter at its narrowest point to the normal internal carotid artery. The degree of stenosis was classified into six groups: no stenosis, mild stenosis (< 30%), moderate stenosis (30% to 70%), severe stenosis (> 70%), near occlusion, and occlusion (100%). No measurement was made in cases of normal artery, near occlusion, and occlusion. RESULTS: Correlations between angiography and the three types of reconstruction were very good. Axial sections correctly classified the carotid arteries in 95% of cases. In 10 carotid arteries, stenosis was not assessable by SSD and MIP because of calcifications. In the remaining carotid arteries, MIP correctly classified the degree of stenosis in 96% of cases, whereas SSD misclassified 21% of cases. CONCLUSIONS: Our study showed that axial images provide a reliable evaluation of carotid artery stenosis. Calcifications are limiting factors in SSD or MIP. When atherosclerotic plaques are not calcified, MIP reconstructions provide a more reliable measurement of the vascular lumen than SSD.

Adult↗
PubMed1995

Multiple cerebral infarcts associated with an atrial septal aneurysm. Superimposed thrombus detected by transesophageal echocardiography.

The authors describe the case of a patient referred for evaluation of multiinfarct dementia. Conventional echocardiography revealed an aneurysm of the interatrial septum. A transesophageal echocardiogram demonstrated superimposed thrombus. This rare cause of systemic emboli can be diagnosed only by transesophageal echocardiography and is of major interest to avoid recurrence of ischemic strokes.

Aged↗
PubMed1995

Histopathologic correlates of white matter changes on MRI in Alzheimer's disease and normal aging.

We investigated the histopathologic correlates of white matter changes in Alzheimer's disease (AD) patients (n = 6) and controls (n = 9) using postmortem MRI. White matter changes were rated on a 0 to 3 scale in 51 regions. Histopathologically, we subjectively rated the loss of myelinated axons in the deep and periventricular white matter, denudation of the ventricular ependyma, gliosis, width of the perivascular spaces, and leptomeningeal congophilic angiopathy; we measured structural changes in the walls of the blood vessels in the white matter in micrometers. The AD brains displayed significantly more white matter hyperintensities on MRI than controls. Histopathologically, the denudation of the ventricular ependyma and the gliosis were significantly more severe in AD than in controls, and there was a trend toward more loss of myelinated axons in the deep white matter in the AD brains (p = 0.07). The MRI abnormalities correlated with the loss of myelinated axons in the deep white matter (r' = 0.37; p < 0.01) and with the denudation of the ventricular lining (r' = 0.54; p < 0.01). We could not find any evidence for arteriolosclerosis, but the mean thickness of the adventitia of the arteries of the deep white matter in AD almost doubled the value in control brains (p = 0.0009). We conclude that white matter abnormalities in AD patients and controls consist of loss of myelinated axons, probably caused by arterial changes and breakdown of the ventricular lining. Since imaging/histopathologic correlation was similar in AD patients and controls, these changes probably represent some form of accelerated aging.

Aged↗
PubMed1995

Autosomal dominant migraine with MRI white-matter abnormalities mapping to the CADASIL locus.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an autosomal dominant cerebral arteriopathy mapped to chromosome 19 and characterized mainly by recurrent subcortical ischemic strokes and extensive white-matter signal abnormalities (WMAs) on magnetic resonance imaging. Other clinical features include migraine attacks and progressive subcortical dementia. Herein, we describe several members of the same family who suffered migraine attacks, mostly with aura, associated with WMAs, segregating with an autosomal dominant pattern of inheritance. One individual had a progressive subcortical dementia with similar WMAs. Although ischemic stroke, one of the hallmarks of CADASIL, was not present in this family, we hypothesized that the present disorder resulted from an alteration of the CADASIL gene. Genetic linkage analysis, using four chromosome 19 markers spanning the CADASIL locus, supports this hypothesis.

Adult↗
PubMed1995

[Cerebral venous thromboses: study of the course].

The management of patients with presumed cerebral venous thrombosis has been recently modified by magnetic resonance imaging and evidence that heparin decreases mortality and morbidity. No large consecutive series of patients with cerebral venous thrombosis has been reported since then. The aim of our study was to determine the prognosis factors of patients with cerebral venous thrombosis. Demographic, clinical and radiological characteristics were recorded in a homogeneous series of 18 consecutive patients with cerebral venous thrombosis collected over a 31-month period. All patients were treated by heparin at the acute stage. We found no difference in demographic, clinical and radiological characteristics of the patients according to the 1-month and 6-month outcome. We only found a tendency towards a better 1-month outcome in younger patients (p = 0.06) and in patients with an isolated intracranial hypertension (2p = 0.06). A long therapeutic delay might be a factor of poor prognosis which might be hidden by a better spontaneous outcome in patients with isolated intracranial hypertension in whom the diagnostic delay is longer. A multicentric study allowing a multivariate analysis may therefore be useful to identify prognosis factors in patients with cerebral venous thrombosis.

Adolescent↗
PubMed1995

[Magnetic resonance imaging in vascular dementia].

The heterogeneity of vascular dementia depends on the cause, size, location and nature of the vascular lesions (36, 62). Magnetic resonance imaging (MRI) techniques are of major interest to detect the vascular origin of dementia: the lack of focal lesions or leukoencephalopathy excludes the vascular origin of dementia (36). Occlusions of large extra-cerebral arteries usually lead to cortical or large subcortical infarcts or both (28). Dementia may be due to multiple infarcts or to a single infarct located in a strategic area (47). Lacunar infarcts are due to the occlusion of one single deep perforator with a thickening of the arterial wall due to lipohyalinosis (25), usually in a patient with arterial hypertension; lacunes are located in a territory supplied by the deep perforators. They appear as hyperintense in T2-weighted sequences and hypo-intense in T1-weighted sequences. Old small hemorrhages have the same appearance than infarcts on CT-scans but their center appears hypo-intense in T2-weighted sequences. In normal subjects, age and arterial hypertension are risk factors for hemispheric white matter hyperintensities (59, 60). Their vascular origin is likely because of the evidence of lesions of the wall of deep perforators (17, 21), their association with lacunes (17, 21, 30, 37) or deep hemorrhages (30, 32, 37), and their frequency in amyloid angiopathy (26). Their prevalence is higher in vascular dementia than in Alzheimer's disease (59). They sometimes fulfill criteria for Binswanger's disease (5). Even after exclusion of predisposing factors they remain frequent in healthy subjects over 50 years (39, 56); however, whether they herald subsequent dementia remains unsettled.(ABSTRACT TRUNCATED AT 250 WORDS)

Alzheimer Disease↗