[Imaging and cerebral ischemia: which studies?].
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Brain Ischemia↗
Biomedical subjects
D Leys
Publications and source records attributed to D Leys.
[Cerebral angiography: a study of complications in 450 consecutive procedures].
PURPOSE: To evaluate all types of complications, both minor and major, associated with modern cerebral angiography. MATERIALS AND METHODS: A prospective study of 450 consecutive cerebral angiographic procedures is reported. RESULTS: One patient (0.2%) died from a cholesterol embolus. In seven patients (1.6%), thromboembolic events occurred within 24 hours after the procedure, leading to transient ischemic symptoms in six and permanent hemiplegia in one. Two patients suffered from acute renal failure (0.4%). Transient cardiac arrhythmias were observed in three patients without consequence on the clinical outcome. Most complications of angiography occurred in patients referred from the neurology department for work-up of stroke syndrome. CONCLUSION: Our results show that morbidity and mortality rates related to the angiographic procedure did not decrease in spite of major improvement of angiographic materiel. Atherosclerosis is the main risk factor for complication. Most of the complications could be avoided by appropriate selection of indications and by using non-invasive techniques such as magnetic resonance angiography or helical CT angiography.
Acute Kidney Injury↗
Preliminary experience using contrast-enhanced MR angiography to assess vertebral artery structure for the follow-up of suspected dissection.
BACKGROUND AND PURPOSE: Important advances have been made recently in MR angiography with the use of contrast medium injection, which has proved valuable for the imaging of vertebral arteries (VAs) obtained during short scanning times. Our purpose was to assess the feasability of contrast-enhanced fast 3D MR angiography for imaging VAs and to evaluate the long-term follow-up of VA dissections. METHODS: Sixteen consecutive patients with 18 angiographically documented VA dissections (seven occlusive dissections and 11 stenotic dissections, including two each with a pseudoaneurysm) were followed up using both contrast-enhanced 3D MR angiography and cervical T1-weighted MR imaging at a median delay of 22 months. Ten patients underwent MR imaging at the acute phase as well, and nine underwent early follow-up angiography at a median delay of 3 months. MR angiographic findings were determined by consensus, focussing on image quality, presence of residual stenosis, luminal irregularities, and occlusion. RESULTS: Of the 32 VAs, a segment of the artery was not assessable on contrast-enhanced MR angiography in each of four small VAs. A central signal void artifact of cervical arteries was seen in one patient and motion artifacts were seen in two, but images could be interpreted. A venous enhancement was detected in 10 of 16 examinations, but this did not prevent image analysis. Ten of 11 stenotic dissections returned to normal, whereas one stenotic dissection progressed to occlusion. Two pseudoaneurysms detected by initial angiography resolved spontaneously; one was revealed only by delayed MR angiography, and one was detected on an early MR angiogram and proved resolved on a late MR angiogram. Of the seven initially occluded VAs, five reopened, with a hairline residual lumen in each of three. CONCLUSION: This preliminary experience showed that contrast-enhanced MR angiography is a promising tool for imaging VAs; it allows the assessment of VA dissection changes over time. Most lesions tended to heal spontaneously, but persisting occlusion or pseudoaneurysm could be detected during the late course.
Adult↗
[Prevention of cerebral ischemia: anti-platelet agents].
Besides the optimal management of risk factors for stroke and carotid surgery, antiplatelet agents are the cornerstone for prevention of cerebral ischaemia. The aim of this overview is to determine their role in the prevention of cerebral ischaemia, from available literature. In primary prevention, the benefit of aspirin has been established only for patients with non-valvular atrial fibrillation and a low risk of cardioembolism, or as an alternative choice of warfarin, and in subjects at high risk of atherosclerosis. In secondary prevention, antiplatelet agents are effective to reduce the risk in patients with ischaemic stroke due to atherosclerosis: aspirin (50 to 1300 mg), ticlopidine (500 mg), clopidogrel (75 mg) and dipyridamole (400 mg) are effective, but the higher levels of risk reduction are obtained with clopidogrel, ticlopidine and the association aspirin--dipyridamole. Aspirin is recommended in most other causes of cerebral ischaemia, except in high risk cardiopathies when anticoagulation is possible. Other domains should still be explored: are antiplatelet agents also effective to reduce the risk of cerebral ischaemia in patients with other causes, especially lipohyalinosis of the deep perforators leading to lacunar infarcts? In daily practice, does prescription follow recommendations? Will it be possible to reproduce the results of the European Stroke Prevention Study (ESPS)2? Are antiplatelet agents other than aspirin effective in non-valvular atrial fibrillation? Are other associations of antiplatelet agents more effective than these agents alone? Finally, what will be the role of new antiplatelet agents in the future?
Arteriosclerosis↗
[Arterial hypertension and cognitive decline].
Arterial hypertension is the leading risk factor for all stroke subtypes. However, its relationship with cognitive decline and dementia is more complex than a simple causal relationship. Cognitive functions are worse in patients with arterial hypertension, especially when the level of education is lower, age higher and arterial hypertension more severe. Arterial hypertension is an independent factor of cognitive decline. It also leads to white matter changes which contribute to the cognitive decline. Longitudinal studies have shown that a higher blood pressure at the age of 70 years is associated with an increased risk of dementia (vascular or Alzheimer) 10 to 15 years later, but blood pressure spontaneously decreases as dementia occurs. Treatments of arterial hypertension decrease the incidence of stroke, but clinical trials are still necessary to determine if they also decrease the incidence of dementia. Preliminary results obtained in elderly subjects with systolic arterial hypertension, support this hypothesis.
Alzheimer Disease↗
[Risk factors and mechanisms of post-stroke dementia].
Stroke significantly increases the risk of dementia in subjects aged 55 years or more. Twenty to 25 p. 100 of patients are demented 5 years after a stroke. Age and supratentorial location of the vascular lesion are risk factors for post-stroke dementia. Volume, left side of the lesion, large middle cerebral artery infarction, lesions of the frontal lobe, second stroke, diabetes, aphasia, clinical features expressing the severity of the stroke event in the acute phase, mitral valve prolapse, atrial fibrillation, depression, concomitant hypoxic/ischemic disorders, and white matter changes have also been found as predictors of dementia. There are many different mechanisms of vascular pathology that may lead to dementia: ischemic or hemorrhagic lesions, large vessel disease including multi-infarct and strategic single infarct, small-vessel disease including lacunes and white matter changes, hypoperfusion.... Post-stroke dementia may not be due only to vascular lesion. Some post-stroke dementias have a progressive onset and course. The cognitive decline may pre-exist to the stroke, even when a dementia is not diagnosed. This suggests a degenerative process. Alzheimer's disease is frequent in ages when the majority of strokes occur. Alzheimer's and vascular diseases share common risk factors such as age, APOE4, hypertension, and smoking. Patients with low MMS scores and AD patients are at risk for stroke. Moreover, white matter changes are associated with stroke and Alzheimer's disease and may contribute to the cognitive decline. Many post-stroke dementias could be multifactorial. Even when vascular lesions and degenerative changes (mainly Alzheimer changes) are not severe enough, no their own, to be the cause of dementia, their summation may reduce the preclinical stage of the degenerative process.
Aged↗
The primary structures of the low-redox potential diheme cytochromes c from the phototrophic bacteria Rhodobacter sphaeroides and Rhodobacter adriaticus reveal a new structural family of c-type cytochromes.
The complete amino acid sequence of the low-redox potential cytochrome c-551.5 from Rhodobacter sphaeroides was determined by automated Edman degradation combined with mass spectroscopy. There are 139 residues and two typical Cys-X-X-Cys-His heme-binding sites. A homologous low-redox potential cytochrome was also sequenced from Rhodobacter adriaticus and was found to contain 126 residues. It is 53% identical to that of Rb. sphaeroides and has two internal deletions of one and five residues. The Rhodobacter diheme cytochromes are 21-24% identical to the translated open reading frame SLL1886 from Synechocystis sp. PCC6801. There are at least two deletions of five and eight residues in the 188-residue cyanobacterial protein. Each of the three cytochromes has more histidines than it needs to bind the two hemes, but conserved histidines located 23 residues after the first heme and 14-19 residues before the second heme are likely to be the sixth heme ligands. There is no evidence for gene doubling and no similarity to any other known cytochromes. The measured helix content of 24% is much less than normal for c-type cytochromes. These proteins thus appear to be representative of an entirely new class of c-type cytochromes.
Amino Acid Sequence↗
[Prognosis of cerebral ischemic accidents].
One of the roles of neurologists is to determine the prognosis in patients with cerebral infarction. However, it remains difficult to determine the prognosis at the individual level. Patients with cerebral infarction are at risk of death, stroke recurrence, intercurrent complications and sequelae. A clinical improvement may occur years after stroke onset, especially for neuropsychological deficits. Predictors of outcome may lead to a more appropriate management of stroke patients and an optimization of the reinsertion.
Brain Ischemia↗
The influence of coincidental vascular pathology on symptomatology and course of Alzheimer's disease.
The aim of this review is to determine the influence of coincidental cerebrovascular pathology on the symptomatology and course of Alzheimer's disease (AD). The link between stroke and AD is probably higher than expected by chance for the following reasons: (i) both pathologies share genetic risk factors such as the epsilon 4 allele of the apolipoprotein E gene; (ii) AD patients have changes in the brain vessels that may lead to either ischemic or hemorrhagic stroke or white matter changes or both; (iii) there is evidence of an increased risk of stroke in AD patients; (iv) there is evidence of a frequent association of AD and stroke at autopsy. Because of the summation of the various types of lesions, stroke lesions may lead to an increase progression of cognitive decline in AD patients. Recognition of a vascular component in a dementia syndrome is therefore useful for the management of AD patients. Whether an optimal management of risk factors for stroke may delay the clinical expression of dementia in patients with preclinical Alzheimer pathology should be evaluated.
Alzheimer Disease↗
Brain-behaviour relationships. Some models and related statistical procedures for the study of brain-damaged patients.
The study of brain-damaged patients provides the opportunity to examine the anatomy of brain functions, and has been renewed by the development of structural neuroimaging. Despite the development of neuroimaging and neuropsychological assessment, major uncertainties persist on the exact delimitation of the brain areas involved in specific processes, and these contribute to the enduring controversies over the effective lesions associated with neuropsychological disorders. These uncertainties are mainly due to the methods used in the study of brain-behaviour relationships, which frequently rely on a group comparison design. The aim of this study was to provide models for the study of brain-behaviour relationships and to assess the reliability of related statistical procedures. In the present work, four theoretical modes of brain-behaviour relationship consistent with neuropsychological data are put forward: unicity, equivalence, association and summation. The first experimental study was based on a simulated population of patients. Lesions associated with the occurrence of a deficit were predetermined according to modes of brain-behaviour relationship and were compared with lesions selected by statistical analysis. The study showed that (i) the group comparison design did not allow determination of the effective lesion, (ii) stepwise regression analysis was sensitive to the relative frequency of lesions, especially when the occurrence of a deficit depended on two lesions, but did not allow determination of the mode of brain-behaviour relationship, and (iii) the classification tree test described the data very satisfactorily and permitted the determination of the mode of brain-behaviour relationships. In order to assess the validity of statistical analyses, a second study was performed in which lesion locations associated with motor weakness in stroke patients were examined. Selected lesions were compared with the anatomy of the human motor system. The study mainly showed that (i) the stepwise regression analysis of selected lesions was not related to the presence of a motor deficit, and (ii) the classification tree test provided perfect agreement with motor weakness predicted by lesion locations and suggested an equivalence mode of brain-behaviour relationship consistent with current neurological knowledge. These studies provide models of brain-behaviour relationships and related statistical procedures that may allow more precise documentation of the anatomy of brain functions and its pathology, and further investigation of the modalities of brain-behaviour relationships.
Behavior↗
Antithrombin, protein C and protein S levels in 127 consecutive young adults with ischemic stroke.
OBJECTIVES: The aim of our study was to evaluate the prevalence of antithrombin, protein C and protein S deficiencies in consecutive ischemic stroke patients under 45. MATERIAL AND METHODS: We studied 127 consecutive patients with a mean age of 34.4 years admitted for an ischemic stroke, over a 2-year period, after exclusion of those with arterial dissection. Antithrombin, protein C and protein S levels were measured in all patients at the acute stage of the ischemic stroke and measurements were repeated in case of abnormality. RESULTS: We found abnormal levels in 9 patients. Seven had an acquired cause of deficiency (pregnancy, oestrogen, acute inflammation). Two had no obvious acquired cause of deficiency but further controls were normal. CONCLUSIONS: Hereditary deficiencies of coagulation inhibitors are rare in ischemic stroke patients under 45 and their systematic detection seems to be of poor interest.
Adolescent↗
Medial temporal lobe atrophy in stroke patients: relation to pre-existing dementia.
OBJECTIVE: The links between stroke and Alzheimer's disease seem to be closer than expected by chance. In a previous study it was shown that up to 16% of patients admitted for stroke had pre-existing dementia. Medial temporal lobe atrophy (MTLA) is strongly associated with Alzheimer's disease. The aim of this study was to determine the prevalence of MTLA and its relation with pre-existing dementia. METHOD: The study was conducted on 170 consecutive stroke patients (87 women; median age 75 years; 152 infarcts), who underwent non-contrast CT with temporal lobe oriented 2 mm contiguous slices at admission. A cut off point of 11.5 mm was used to differentiate patients with and without MTLA. Pre-existing dementia was assessed using the informant questionnaire on cognitive decline in the elderly (IQCODE) with a cut off score of 104. RESULTS: Ninety four patients (55.3%) had MTLA, of whom 23 (24.5%) had pre-existing dementia; of 76 patients without MTLA, only four (5.3%) had pre-existing dementia (p=0.0007). The logistic regression analysis with MTLA as dependent variable found the following independent variables: increasing age (p<0.05), and global cerebral atrophy scores (p<0.01). The IQCODE scores just reached significance (p=0.05). CONCLUSION: Stroke patients with MTLA are more likely to have pre-existing dementia; this suggests that Alzheimer's disease might contribute to the dementia syndrome. A longitudinal follow up is now necessary to determine whether stroke patients with MTLA and without pre-existing dementia are at increased risk of Alzheimer's disease over subsequent years.
Adult↗
Dystonia after striatopallidal and thalamic stroke: clinicoradiological correlations and pathophysiological mechanisms.
OBJECTIVE: To establish the pathophysiological mechanisms of striatopallidal and thalamic dystonia. METHODS: Five patients from among 26 who presented (between March 1987 and July 1996) with focal dystonia, segmental dystonia, or hemidystonia caused by a single localised vascular lesion, were selected. Patients with lesions with indefinite boundaries, and diffuse, or multiple, or large brain lesions were excluded. Three dimensional T1 weighted MRI (1.5 tesla) was performed to determine the topography of the lesions. The atlas of Hassler allowed the stereotactic localisation of the lesions to be specified exactly. RESULTS: Three patients had dystonic spasms associated with striatopallidal lesions and one with a thalamic and striatopallidal lesion. One other patient presented with a myoclonic dystonia related to a thalamic lesion. The striatopallidal lesions were located in the sensorimotor area with a somatotopical distribution. The pure thalamic lesion involved the centromedian nucleus, the sensory nuclei, and the pulvinar whereas the thalamic and striatopallidal lesion was located in the pallidonigral thalamic territory, which receives pallidonigral inputs. CONCLUSION: The striatopallidal dystonia might be the consequence of the interruption of the cortico-striato-pallido-thalamo-cortical loop induced by lesions located within the sensorimotor part of the striatopallidal complex. By contrast, it is suggested that thalamic dystonia might be caused by lesions located in the centro-median or the ventral intermediate nuclei, outside the pallidonigral territory, but leading also to a dysfunction of the cortico-striato-pallido-thalamo-cortical loop.
Adult↗
White matter changes on CT and MRI: an overview of visual rating scales. European Task Force on Age-Related White Matter Changes.
Since the recognition of white matter changes on CT (leukoaraiosis), rating scales for the location and severity of white matter changes have been developed, mainly for research purposes, to investigate factors such as the relation with cognition, risk factors, and pathology. The main purpose of rating scales is to provide scores that can be used in statistical analyses. The development of the NINDS-AIREN criteria for vascular dementia have introduced a new application for these rating scales in investigating and delineating the amount of white matter changes on CT/MRI sufficient to fulfill the criteria. Furthermore, in Alzheimer's disease, recognition of white matter changes may serve to delineate homogeneous groups and help to identify patients with different symptomatology. We reviewed the existing rating scales for CT and MRI and judged their properties and reliability. The ideal rating scale does not yet exist, but different rating scales may serve different purposes, for which some recommendations are made.
Brain Ischemia↗
White matter changes and poststroke dementia.
Stroke patients are more likely to have white matter changes than age- and sex-matched controls. White matter changes are associated with an increased risk of dementia occurring after stroke: they often indicate a higher risk of stroke recurrence and they may lead to slight cognitive impairment. Besides white matter changes, vascular lesions of the brain and associated Alzheimer pathology, the summation of 2 or 3 of these mechanisms may lead to dementia in stroke patients even when each type of lesion is not severe enough to induce dementia by its own.
Brain↗
Cerebral magnetic resonance imaging in patients with or without antiphospholipid antibodies.
OBJECTIVE: To determine in patients with systemic lupus erythematosus (SLE) or with primary antiphospholipid syndrome (PAPS) the prevalence of cerebral magnetic resonance imaging changes (MRI) and the relationship with antiphospholipid antibodies. METHODS: Twenty-nine consecutive SLE patients, 24 PAPS patients and 31 healthy controls were prospectively included in the study and underwent MRI Scan over a 1-year period. MRI scans were analyzed separately by a neuroradiologist for white matter changes [periventricular hyperintensity (PVH) (0-6 scale), deep white matter hyperintensity (WMH) (0-24 scale)], and one neurologist for cerebral atrophy (0-39 scale) and stroke subtypes. Statistical assessment consisted of a discriminant analysis performed with SAS-package with MRI data as dependent variables and, as independent variables, age, sex, arterial hypertension, diabetes mellitus, cardiopathy, migraine, neurological symptoms, antiphospholipid antibodies, SLE, steroid treatment. RESULTS: The prevalence of cerebral atrophy was increased in both SLE and PAPS groups relative to controls. PVH and WMH scores were significantly higher in SLE and PAPS than in controls. Focal infarct did not differ in the SLE group when compared with PAPS. PVH and WMH scores were significantly higher in patients with neurological symptoms. Using a correlation test we found a weak significant correlation between cerebral atrophy and lupus anticoagulant. The multivariate analysis found only three independent variables related to PVH and WMH: age, the diagnosis of SLE and cerebral atrophy. CONCLUSIONS: Age, presence of SLE and presence of neurological symptoms were independently related with WMH and PVH, but not antiphospholipid antibodies.
Adolescent↗
Creutzfeldt-Jakob disease: neurophysiologic visual impairments.
OBJECTIVE: The predictive value of electrophysiologic visual testing in Creutzfeldt-Jakob disease (CJD) was investigated, and the retinal pathologic findings in three cases are reported. BACKGROUND: The fatal prognosis of CJD, its transmissibility, and the lack of treatment make early diagnosis essential in averting human-to-human transmission. Electroretinogram and visual evoked potentials have been studied in few cases of CJD. METHODS: A visual electrophysiologic examination was performed in 41 consecutive patients referred with suspected CJD. The disease had been diagnosed in 24 patients (CJD group; 15 were confirmed neuropathologically and 9 by clinicolaboratory methods in accordance with diagnostic criteria). The remaining 17 patients were diagnosed with other neurologic disorders, and served as a control group. RESULTS: Flash electroretinogram revealed a significant decrease in the amplitude of the B1 wave (<60 microV) and the B/A ratio (<2) in the CJD group compared with those in the control group. Flash visual evoked potentials revealed no significant difference in latency, but amplitude was increased (>10 microV) in the CJD group, especially in patients with myoclonus. CONCLUSIONS: The visual electrophysiologic abnormalities provide an interesting noninvasive diagnostic tool in idiopathic CJD. The B1-wave decrease is closely correlated with the outer plexiform layer abnormalities observed on neuropathologic examination.
Adult↗
Helical CT for the follow-up of cervical internal carotid artery dissections.
PURPOSE: The aim of this study was to assess the changes over time of internal carotid artery (ICA) dissections by using helical CT. METHODS: Twenty-seven patients with 30 angiographically proved ICA dissections were followed up with helical CT at 7 to 62 months (median, 24 months) after conventional angiography. CT scans, analyzed independently by two radiologists in a blinded fashion, were evaluated for the presence of mural thickening, aneurysmal formation, and arterial occlusion. In cases without persisting occlusion or aneurysm, we measured the external diameter of the ICA at its upper segment. RESULTS: The interobserver agreement was good. Mild mural thickening was observed in four cases of 30 previously dissected ICAs. All stenotic and nearly occlusive dissections without an aneurysm (n = 12) reverted to a normal or nearly normal diameter. Half the aneurysms resolved spontaneously (four of eight). Of the 10 occluded ICAs, nine were recanalized, but their external diameter was significantly smaller than that of normal carotid arteries, and a hypoplastic appearance was seen throughout the cervical segment of the ICA in three cases. CONCLUSION: Most arterial lesions tend to improve or disappear spontaneously, but persisting ICA narrowing may be observed in the late course of occlusive-type dissections.
Adult↗