Dementia in stroke.
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Biomedical subjects
Publications and source records attributed to O Godefroy.
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The aim of this study is to investigate general intellectual and memory performances at the secondary (3 weeks to 4.5 months) and late (10 to 16 months) stages following rupture of anterior communicating artery aneurysms (AACA). Twenty one patients presenting with selective lesion within frontal, or cingulate, callosal, caudate, basal forebrain areas were evaluated. At the secondary stage, the analysis of the general intellectual capacities revealed a drop of performance, prominent on performance IQ, which was more severe than the learning deficit. Specific cognitive evaluations revealed increase of the execution time, but performance was relatively preserved: in the Stroop test, focused attention disorder was moderate: the modified Wisconsin Card Sorting test was correctly performed in most cases; significant deficits of verbal short-term memory, long-term verbal and visuo-spatial learning, and access to semantic memory were observed. At the late stage, general intellectual performance improved, but did not reached the estimated prelesional level in most cases; specific cognitive disorders had most often disappeared. Most performances were best explained by the severity of lesions in the left cingulate cortex and corpus callosum area. These results show that the cognitive profile of AACA patients is different from classical descriptions of the "amnesic syndrome", and is also different at the secondary and late stages; this evolution has to be taken into account in studies describing cognitive deficits of such patients, or comparing them with others presenting with "annesic syndrome".
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.
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.
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.
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.
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The term subcortical dementia suggests that the cerebral lesions critical for the occurrence of dementia are located in subcortical structures. Accordingly, these dementias are usually observed in patients suffering from degenerative disorders affecting subcortical structures. They are characterised by neuropsychological and behavioral disorders resembling those observed in lesion of the prefrontal cortex. Numerous reports suggest that patients suffering from degenerative and focal lesions of the striatum exhibit an impairment of the so-called "frontal functions". These results support the hypothesis that the striatum is involved in these functions and therefore, that its lesion might account for the neuropsychological disorders. The interpretation of these results assumes that cerebral lesions are restricted to the striatum. However, recent studies have shown that lesions of degenerative and vascular disorders of the striatum frequently extend into the cortex. Moreover, assessment of patients with striatal infarct has shown that the occurrence of frontal lobe symptoms depended on the associated cortical lesion and that patients with pure striatal lesion did not exhibit a full dysexecutive syndrome. The contribution of the striatum to frontal lobe functions might thus have been overestimated. Despite the uncertainty about the critical locus of lesions accounting for the emergence of dementia, the term subcortical dementia has the advantage to refer to a group of dementias with a specific neuropsychological pattern. A much more relevant approach would be to evaluate the contribution of the striatum to the executive functions. In keeping with this view, recent studies suggest that the caudate nucleus is mainly involved in response selection, at least in unusual or complex tasks.
The higher sensitivity of chronometric analysis leads to an increase of their use in the evaluation of brain-damaged patients. However, patients have usually higher reaction time (RT) variability, suggesting a possible decrease in the reliability of RT measurement. This reliability has never been evaluated in patients. This study assessed the reliability of RT estimates in 2 populations of brain-damaged patients and controls, using the Kendall coefficient of concordance W. Concordance coefficients were computed for simple detection and choice tests. W values were good and significant. This study suggests that RT measured in simple detection and choice tasks represent a reliable measurement and supports the idea that the higher sensitivity associated with the use of chronometric analysis is not obtained at the cost of a lower reliability. Moreover, these results provide information for the elaboration of RT tests.
Despite the wide use of RT tests in brain-damaged patients assessment, effects of the level of vigilance, fatigability, practice and motivation on RT have been poorly investigated. We assessed vigilance and effects of fatigability, practice and motivation on brain-damaged patients suffering from lesion of the prefrontal cortex prominent in basofrontal areas and controls using simple RT tests. Our study showed fatigability and practice effects which did not affect RT differences between groups, whereas motivation effect was not significant. Finally, patients did not suffer from a deficit of vigilance. These results suggest that the attentional disorders demonstrated in the same patient group were related neither to a higher sensitivity to fatigability nor to an insufficient practice.
Atrial septal aneurysms (ASA) are frequent findings on transesophageal echocardiographies. Whether they are more frequent in patients with cerebral ischemia of unknown cause remains unclear. We investigated this question in 154 consecutive patients with an ischemic stroke or transient ischemic attack. The 16 patients with ASA were younger, less likely to have arterial hypertension and more likely to have a patent foramen ovale (PFO) or an unknown cause of stroke, but they did not differ for number and side of infarcts, other demographic data and vascular risk factors. Patients with ASA unassociated to PFO were also more likely to have an unknown cause of stroke. These findings lead to the hypothesis that ASA might be sources of cerebral emboli.
According to previous studies, focal capsulostriatal lesions may produce aphasia, hemineglect, gestural apraxia, frontal lobe dysfunction, and memory impairment. A few reports of capsulostriate infarcts secondary to involvement of lenticulostriate arteries have confirmed that aphasia and hemineglect may occur whereas gestural apraxia, anosognosia and frontal-lobe symptoms are rare. Most studies used CT scan assessment and did not exclude possible associated lesions. Neuropsychological changes in 11 patients with lenticulostriate infarcts diagnosed by CT scan were prospectively investigated. MRI in five of the 11 patients showed an associated cortical lesion not seen on CT scan. Patients with pure lenticulostriate infarcts on MRI may exhibit aphasia of mild severity whereas Broca's aphasia, hemineglect, gestural apraxia, and anosognosia were only seen in the subgroup with associated cortical lesions. Aphasia in patients with pure lenticulostriate infarcts was characterised by prominent expressive and lexicosemantic task impairments. The results strongly suggest that cortical involvement is critical to the extent and severity of neuropsychological changes in patients with lenticulostriate infarcts.
Whether watershed infarcts and internal junctional infarcts have different mechanisms remains unknown. Of 493 consecutive patients with ischemic stroke or transient ischemic attack, 26 had 1 watershed infarct or more (8 anterior and 21 posterior) and 18 had 1 internal junctional infarct or more. Patients with watershed infarcts were more likely to have arterial hypertension [95% confidence intervals of odds ratio (CIOR): 1.04-6.15] and internal carotid artery stenosis > 50% (95% CIOR: 1.03-7.12) than patients without borderzone infarcts. Patients with internal junctional infarcts were more likely to have heart diseases than patients without borderzone infarcts (95% CIOR: 1.46-10.52). This preliminary study suggests that both subtypes of borderzone infarcts probably have different mechanisms.
Pure sensory strokes (PSS) are usually due to thalamic lacunar infarcts. We report a case of PSS in a 34-year-old female suffering from migraine who complained of sudden isolated left-sided paresthesia involving face, upper and lower limbs. We found a complex vascular abnormality associating internal carotid artery occlusion, posterior cerebral artery agenesia, aneurysm at the posterior face of the carotid siphon and angiomatous rete at the top of the basilar artery. The acquired origin of the carotid artery occlusion by possible neonatal dissection is probable since this patient has a permeable carotid canal on CT scan.
BACKGROUND AND PURPOSE: Possible specific risk factors for silent infarcts remain unknown. The aim of this study was to investigate whether risk factors for silent infarcts differ from those for symptomatic infarcts in stroke patients. METHODS: Silent infarcts were defined as asymptomatic infarcts detected on computed tomographic scan in patients free of history of stroke and unrelated to the symptoms and signs of the index stroke. Of 595 consecutive patients with stroke or transient ischemic attacks, 116 (19%) had at least one silent infarct on the first computed tomographic scan performed within 24 hours after onset. They were compared with the 479 remaining patients for cerebrovascular risk factors and for presumed mechanism of stroke by means of the odds ratio method. A discriminant analysis was then performed in the subgroup of 216 patients with ischemic stroke who underwent an exhaustive cardiac and vascular workup. RESULTS: One hundred forty-one silent infarcts (99% confidence interval [CI], 29% to 41%) and 265 symptomatic infarcts (99% CI, 59% to 71%) were subcortical infarcts smaller than 15 mm. Univariate analysis showed that patients with silent infarcts were more likely to be older than 65 years (odds ratio [99% CI], 1.11 to 3.49) and to have left atrial enlargement on echocardiogram (odds ratio [99% CI], 1.02 to 26.70) and leukoaraiosis (odds ratio [99% CI], 1.39 to 4.21). Discriminant analysis found only two independent risk factors for silent infarcts: left atrial enlargement (P = .007) and age older than 65 years (P = .03); leukoaraiosis was not found to be an independent risk factor (P = .86). CONCLUSIONS: Age and left atrial enlargement are the main risk factors for silent infarcts in patients with ischemic stroke or transient ischemic attacks.
Most studies on frontal lobe dysfunction (FLD) in patients with striatal lesions did not consider possible associated cortical lesions not seen on computed tomographic scans. To determine the possible role of such cortical lesions, we assessed FLD in 10 patients with unilateral lenticulostriate infarct on computed tomographic scans. Magnetic resonance imaging revealed an associated cortical infarct not seen on computed tomographic scans in four patients. Using a battery of neuropsychological tests sensitive to FLD, we found that (1) the crossed tapping test was the only FLD test significantly disturbed in patients with pure unilateral lenticulostriate infarcts, (2) FLD was only present in patients with associated cortical infarct, and (3) caudate lesions only account for the number of echopraxic errors in the crossed tapping test. We conclude that unilateral isolated lenticulostriate infarcts might not lead to FLD, even though they may disturb the development of strategies involved in motor procedural learning.
BACKGROUND AND PURPOSE: Early noncontrast computed tomographic scans may visualize a hyperdense middle cerebral artery before the infarct becomes visible. This sign disappears within a few days, corresponds to the clot itself, and might be associated with a poor prognosis. The aim of the study was to determine its prevalence, diagnostic value, relationship to demographic data, ability to separate embolic from nonembolic causes, short-term prognostic value, evolution over time, and relationship to arterial occlusion on angiography. METHODS: We performed this study using computed tomographic scans performed within 12 hours after onset in 272 consecutive unselected patients with a first acute cerebrovascular event. RESULTS: Seventy-three subjects had the hyperdense middle cerebral artery sign, leading to a prevalence of 26.8% in the whole group and 41.2% in patients with a middle cerebral artery infarct. Specificity was 100%, but sensitivity was only 30%. This sign was not dependent on cerebrovascular risk factors, but was more likely to occur in cortical and in large, deep, middle cerebral artery infarcts (p less than 0.01). It provided only a 3.5% gain in predicting death, and one fifth of patients with the sign recovered within 2 weeks; this sign was not an independent variable of poor outcome on multiple linear regression. It spontaneously disappeared within a few days and was always related to an occlusion of the middle cerebral artery in patients who underwent early angiography. CONCLUSIONS: The hyperdense middle cerebral artery sign is useful in the diagnosis of middle cerebral artery occlusion but does not always predict a poor prognosis.
We report a new case of neuromuscular block overlap between Myasthenia Gravis and Eaton-Lambert syndrome. A 64-year-old man with a 4-months history of gait disturbance was admitted for ophthalmoplegia worsening during exercise and decreasing at rest. Clinical examination after exercise, revealed limbs weakness and areflexia, palsy of the left eye abduction and a left ptosis. The level of anti-acetylcholin-receptor antibodies was high. Electrophysiological explorations revealed a decrement at 3 Hz and a increment at 30 Hz, with a reduction in amplitude of the initial motor potential. This patient improved under a combination of guanidine and anticholinesterase drugs. From this case and 9 previously reported cases, we propose 4 criteria for the diagnosis of such neuromuscular blocks: 1) exercising symptoms and signs, including areflexia, 2) presence of anti-acetylcholin-receptor antibodies, 3) reduction of the amplitude of the initial motor potential, with a decrement at 3 Hz, and an increment at 30 Hz, and 4) clinical and electrophysiological improvement under guanidine and anticholinesterasic drugs therapy.